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Dr Nicole Hansbro

Conjoint Fellow

School of Biomedical Sciences and Pharmacy (Immunology and Microbiology)

Career Summary

Biography

Research Expertise
I have established a mouse model of viral infection employing a rodent specific virus, which is the only such model in Australia. The model employs infection with a natural mouse pathogen, which induces natural virus-host interactions. I have developed this model in both neonatal and adult mice and have investigated the effects of respiratory viruses on whole mammal immune responses and predisposition/exacerbation of asthma. Briefly, a non-lethal PVM infection in adult mice induces pathologic features associated with viral associated asthma, namely a neutrophilic, mild eosinophilic influx into the lungs, expansion of CD8+ and CD4+ T cells, goblet cell hyperplasia, and airways hyper-responsiveness. Peak viral titre within the lungs occurs 6 days post infection (dpi), and precedes the peak inflammatory response which occurs 12 dpi and is characterised by CD8 T cell derived IFN-¿, neutrophils, monocytes, and mucus hyperplasia. As the inflammatory response resolves, cytokine production from polyclonally stimulated splenocytes switches from IFN-¿ to IL-13 (produced from CD4+ T cells). Interestingly, neonatal mice are not susceptible to a lethal PVM infection and are further protected from infection later in life. The immune response to re-infection is characterized by a lymphocytic and eosinophilic influx into the lungs, mucus cell hyperplasia, and a predominantly IFN-¿ response form CD8+ T cells despite the failure of the CD8+ T cells to expand upon re-infection. Recently we have also observed for the first time that angiogenesis (new blood vessel formation) occurs in the neonatal model of viral infection. Angiogenesis has also been widely associated with the development of asthma.

Qualifications

  • PhD, University of Newcastle
  • Bachelor of Science (Honours), University of Newcastle

Keywords

  • allergy
  • asthma
  • mouse models
  • virus

Fields of Research

Code Description Percentage
110799 Immunology not elsewhere classified 70
111799 Public Health and Health Services not elsewhere classified 10
110299 Cardiorespiratory Medicine and Haematology not elsewhere classified 20

Professional Experience

Academic appointment

Dates Title Organisation / Department
1/03/2003 -  Post-doctoral fellow Australian National University
Australia
1/01/2003 - 1/01/2007 Post-doctoral fellow University of Newcastle
School of Biomedical Sciences and Pharmacy
Australia
1/01/1998 - 1/01/1999 Research Assistant University of Newcastle
Australia
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Publications

For publications that are currently unpublished or in-press, details are shown in italics.


Journal article (37 outputs)

Year Citation Altmetrics Link
2019 Ng SW, Chan Y, Chellappan DK, Madheswaran T, Zeeshan F, Chan YL, et al., 'Molecular modulators of celastrol as the keystones for its diverse pharmacological activities', Biomedicine and Pharmacotherapy, 109 1785-1792 (2019)

© 2018 The Authors In the recent years, much attention has been focused on identifying bioactive compounds from medicinal plants that could be employed in therapeutics, which is a... [more]

© 2018 The Authors In the recent years, much attention has been focused on identifying bioactive compounds from medicinal plants that could be employed in therapeutics, which is attributed to their potent pharmacological actions and better toxicological profile. One such example that has come into the light with considerable interest is the pentacyclic triterpenoid, celastrol, which has been found to provide substantial therapeutic properties in a variety of diseases. In an effort to further accelerate its potential to be utilized in clinical practice in the future; along with advancing technologies in the field of drug discovery and development, different researchers have been investigating on the various mechanisms and immunological targets of celastrol that underlie its broad spectrum of pharmacological properties. In this review, we have collated the various research findings related to the molecular modulators responsible for different pharmacological activities shown by celastrol. Our review will be of interest to the herbal, biological, molecular scientist and by providing a quick snapshot about celastrol giving a new direction in the area of herbal drug discovery and development.

DOI 10.1016/j.biopha.2018.11.051
Co-authors Peter Wark, Alan Hsu, Philip Hansbro
2018 Shastri MD, Shukla SD, Chong WC, Dua K, Peterson GM, Patel RP, et al., 'Role of Oxidative Stress in the Pathology and Management of Human Tuberculosis', OXIDATIVE MEDICINE AND CELLULAR LONGEVITY, 2018 (2018) [C1]
DOI 10.1155/2018/7695364
Co-authors Philip Hansbro
2018 Dua K, Hansbro NG, Foster PS, Hansbro PM, 'Targeting MicroRNAs: Promising Future Therapeutics in the Treatment of Allergic Airway Disease', CRITICAL REVIEWS IN EUKARYOTIC GENE EXPRESSION, 28 125-127 (2018)
DOI 10.1615/CritRevEukaryotGeneExpr.2018022218
Co-authors Philip Hansbro, Paul Foster
2018 Ng ZY, Wong JY, Panneerselvam J, Madheswaran T, Kumar P, Pillay V, et al., 'Assessing the potential of liposomes loaded with curcumin as a therapeutic intervention in asthma', Colloids and Surfaces B: Biointerfaces, 172 51-59 (2018) [C1]

© 2018 Elsevier B.V. Curcumin a component of turmeric, which is derived from Curcuma longa is used as a colouring agent and as a dietary spice for centuries. Extensive studies hav... [more]

© 2018 Elsevier B.V. Curcumin a component of turmeric, which is derived from Curcuma longa is used as a colouring agent and as a dietary spice for centuries. Extensive studies have been done on the anti-inflammatory activity of curcumin along with its molecular mechanism involving different signalling pathways. However, the physicochemical and biological properties such as poor solubility and rapid metabolism of curcumin have led to low bioavailability and hence limits its application. Current therapies for asthma such as bronchodilators and inhaled corticosteroids (ICS) are aimed at controlling disease symptoms and prevent asthma exacerbation. However, this approach requires lifetime therapy and is associated with a constellation of side effects. This creates a clear unmet medical need and there is an urgent demand for new and more-effective treatments. The present study is aimed to formulate liposomes containing curcumin and evaluate for its anti-inflammatory effects on lipopolysaccharide (LPS)-induced inflammation on BCi-NS1.1 cell line. Curcumin and salbutamol liposomes were formulated using lipid hydration method. The prepared liposomes were characterized in terms of particle size, zeta potential, encapsulation efficiency and in-vitro release profile. The liposomes were tested on BCI-NS1.1 cell line to evaluate its anti-inflammatory properties. The various pro-inflammatory markers studied were Interleukin-6 (IL-6), Interleukin-8 (IL-8), Interleukin-1ß (IL-1ß) and Tumour Necrosis Factor-a (TNF-a). Additionally, molecular mechanics simulations were used to elucidate the positioning, energy minimization, and aqueous dispersion of the liposomal architecture involving lecithin and curcumin. The prepared curcumin formulation showed an average size and zeta potential of 271.3 ± 3.06 nm and -61.0 mV, respectively. The drug encapsulation efficiency of liposomal curcumin is 81.1%. Both curcumin-loaded liposomes formulation (1 µg/mL, 5 µg/mL) resulted in significant (p < 0.05) reduction in the level of pro-inflammatory marker expression such as IL-6, IL-8, IL-1ß and TNF-a compared to positive control group. Liposomal curcumin with the dose of 1 µg/mL reduced the inflammatory markers more effectively compared to that of 5 µg/mL. Liposomal curcumin could be a promising intervention for asthma therapy showing their efficacy in suppressing the important pro-inflammatory markers involved in the pathogenesis of asthma.

DOI 10.1016/j.colsurfb.2018.08.027
Citations Scopus - 1
Co-authors Alan Hsu, Philip Hansbro, Peter Wark
2018 Chellappan DK, Ng ZY, Wong JY, Hsu A, Wark P, Hansbro N, et al., 'Immunological axis of curcumin-loaded vesicular drug delivery systems', Future Medicinal Chemistry, 10 839-844 (2018) [C1]

© 2018 Newlands Press. Several vesicular systems loaded with curcumin have found their way in the therapeutic applications of several diseases, primarily acting through their immu... [more]

© 2018 Newlands Press. Several vesicular systems loaded with curcumin have found their way in the therapeutic applications of several diseases, primarily acting through their immunological pathways. Such systems use particles at a nanoscale range, bringing about their intended use through a range of complex mechanisms. Apart from delivering drug substances into target tissues, these vesicular systems also effectively overcome problems like insolubility and unequal drug distribution. Several mechanisms are explored lately by different workers, and interest over vesicular curcumin has been renewed in the past decade. This commentary discusses several immunological targets in which curcumin is employed in a vesicular form.

DOI 10.4155/fmc-2017-0245
Citations Scopus - 3Web of Science - 1
Co-authors Peter Wark, Alan Hsu, Philip Hansbro
2017 Foster PS, Maltby S, Rosenberg HF, Tay HL, Hogan SP, Collison AM, et al., 'Modeling T

© 2017 John Wiley &amp; Sons A/S. Published by John Wiley &amp; Sons Ltd In this review, we highlight experiments conducted in our laboratories that have elucidated functional... [more]

© 2017 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd In this review, we highlight experiments conducted in our laboratories that have elucidated functional roles for CD4+ T-helper type-2 lymphocytes (TH2 cells), their associated cytokines, and eosinophils in the regulation of hallmark features of allergic asthma. Notably, we consider the complexity of type-2 responses and studies that have explored integrated signaling among classical TH2 cytokines (IL-4, IL-5, and IL-13), which together with CCL11 (eotaxin-1) regulate critical aspects of eosinophil recruitment, allergic inflammation, and airway hyper-responsiveness (AHR). Among our most important findings, we have provided evidence that the initiation of TH2 responses is regulated by airway epithelial cell-derived factors, including TRAIL and MID1, which promote TH2 cell development via STAT6-dependent pathways. Further, we highlight studies demonstrating that microRNAs are key regulators of allergic inflammation and potential targets for anti-inflammatory therapy. On the background of TH2 inflammation, we have demonstrated that innate immune cells (notably, airway macrophages) play essential roles in the generation of steroid-resistant inflammation and AHR secondary to allergen- and pathogen-induced exacerbations. Our work clearly indicates that understanding the diversity and spatiotemporal role of the inflammatory response and its interactions with resident airway cells is critical to advancing knowledge on asthma pathogenesis and the development of new therapeutic approaches.

DOI 10.1111/imr.12549
Citations Scopus - 12Web of Science - 7
Co-authors Hock Tay, Paul Foster, Steven Maltby, Joerg Mattes, Philip Hansbro, Ming Yang, Adam Collison, Gerard Kaiko
2017 Hansbro PM, Kim RY, Starkey MR, Donovan C, Dua K, Mayall JR, et al., 'Mechanisms and treatments for severe, steroid-resistant allergic airway disease and asthma', Immunological Reviews, 278 41-62 (2017) [C1]

© 2017 John Wiley &amp; Sons A/S. Published by John Wiley &amp; Sons Ltd Severe, steroid-resistant asthma is clinically and economically important since affected individuals d... [more]

© 2017 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd Severe, steroid-resistant asthma is clinically and economically important since affected individuals do not respond to mainstay corticosteroid treatments for asthma. Patients with this disease experience more frequent exacerbations of asthma, are more likely to be hospitalized, and have a poorer quality of life. Effective therapies are urgently required, however, their development has been hampered by a lack of understanding of the pathological processes that underpin disease. A major obstacle to understanding the processes that drive severe, steroid-resistant asthma is that the several endotypes of the disease have been described that are characterized by different inflammatory and immunological phenotypes. This heterogeneity makes pinpointing processes that drive disease difficult in humans. Clinical studies strongly associate specific respiratory infections with severe, steroid-resistant asthma. In this review, we discuss key findings from our studies where we describe the development of representative experimental models to improve our understanding of the links between infection and severe, steroid-resistant forms of this disease. We also discuss their use in elucidating the mechanisms, and their potential for developing effective therapeutic strategies, for severe, steroid-resistant asthma. Finally, we highlight how the immune mechanisms and therapeutic targets we have identified may be applicable to obesity-or pollution-associated asthma.

DOI 10.1111/imr.12543
Citations Scopus - 10Web of Science - 7
Co-authors Gang Liu, Philip Hansbro, Lisa Wood, Jay Horvat, Jodie Simpson, Darryl Knight, Chantal Donovan, Malcolm Starkey, Paul Foster
2017 Nair PM, Starkey MR, Haw TJ, Liu G, Horvat JC, Morris JC, et al., 'Targeting PP2A and proteasome activity ameliorates features of allergic airway disease in mice', Allergy: European Journal of Allergy and Clinical Immunology, 72 1891-1903 (2017) [C1]

© 2017 EAACI and John Wiley and Sons A/S. Published by John Wiley and Sons Ltd. Background: Asthma is an allergic airway disease (AAD) caused by aberrant immune responses to aller... [more]

© 2017 EAACI and John Wiley and Sons A/S. Published by John Wiley and Sons Ltd. Background: Asthma is an allergic airway disease (AAD) caused by aberrant immune responses to allergens. Protein phosphatase-2A (PP2A) is an abundant serine/threonine phosphatase with anti-inflammatory activity. The ubiquitin proteasome system (UPS) controls many cellular processes, including the initiation of inflammatory responses by protein degradation. We assessed whether enhancing PP2A activity with fingolimod (FTY720) or 2-amino-4-(4-(heptyloxy) phenyl)-2-methylbutan-1-ol (AAL(S)), or inhibiting proteasome activity with bortezomib (BORT), could suppress experimental AAD. Methods: Acute AAD was induced in C57BL/6 mice by intraperitoneal sensitization with ovalbumin (OVA) in combination with intranasal (i.n) exposure to OVA. Chronic AAD was induced in mice with prolonged i.n exposure to crude house dust mite (HDM) extract. Mice were treated with vehicle, FTY720, AAL(S), BORT or AAL(S)+BORT and hallmark features of AAD assessed. Results: AAL(S) reduced the severity of acute AAD by suppressing tissue eosinophils and inflammation, mucus-secreting cell (MSC) numbers, type 2-associated cytokines (interleukin (IL)-33, thymic stromal lymphopoietin, IL-5 and IL-13), serum immunoglobulin (Ig)E and airway hyper-responsiveness (AHR). FTY720 only suppressed tissue inflammation and IgE. BORT reduced bronchoalveolar lavage fluid (BALF) and tissue eosinophils and inflammation, IL-5, IL-13 and AHR. Combined treatment with AAL(S)+BORT had complementary effects and suppressed BALF and tissue eosinophils and inflammation, MSC numbers, reduced the production of type 2 cytokines and AHR. AAL(S), BORT and AAL(S)+BORT also reduced airway remodelling in chronic AAD. Conclusion: These findings highlight the potential of combination therapies that enhance PP2A and inhibit proteasome activity as novel therapeutic strategies for asthma.

DOI 10.1111/all.13212
Citations Scopus - 2Web of Science - 2
Co-authors Nikki Verrills, Malcolm Starkey, Philip Hansbro, Jay Horvat, Gang Liu
2017 Dua K, Hansbro NG, Hansbro PM, 'STEROID RESISTANCE AND CONCOMITANT RESPIRATORY INFECTIONS: A CHALLENGING BATTLE IN PULMONARY CLINIC', EXCLI JOURNAL, 16 981-985 (2017)
DOI 10.17179/excli2017-425
Co-authors Philip Hansbro
2017 Kim RY, Horvat JC, Pinkerton JW, Starkey MR, Essilfie AT, Mayall JR, et al., 'MicroRNA-21 drives severe, steroid-insensitive experimental asthma by amplifying phosphoinositide 3-kinase¿mediated suppression of histone deacetylase 2', Journal of Allergy and Clinical Immunology, 139 519-532 (2017) [C1]

© 2016 American Academy of Allergy, Asthma &amp; Immunology Background Severe steroid-insensitive asthma is a substantial clinical problem. Effective treatments are urgently req... [more]

© 2016 American Academy of Allergy, Asthma & Immunology Background Severe steroid-insensitive asthma is a substantial clinical problem. Effective treatments are urgently required, however, their development is hampered by a lack of understanding of the mechanisms of disease pathogenesis. Steroid-insensitive asthma is associated with respiratory tract infections and noneosinophilic endotypes, including neutrophilic forms of disease. However, steroid-insensitive patients with eosinophil-enriched inflammation have also been described. The¿mechanisms that underpin infection-induced, severe steroid-insensitive asthma can be elucidated by using mouse models of disease. Objective We sought to develop representative mouse models of severe, steroid-insensitive asthma and to use them to identify pathogenic mechanisms and investigate new treatment approaches. Methods Novel mouse models of Chlamydia, Haemophilus influenzae, influenza, and respiratory syncytial virus respiratory¿tract infections and ovalbumin-induced, severe, steroid-insensitive allergic airway disease (SSIAAD) in BALB/c mice were developed and interrogated. Results Infection induced increases in the levels of microRNA (miRNA)-21 (miR-21) expression in the lung during SSIAAD, whereas expression of the miR-21 target phosphatase and tensin homolog was reduced. This was associated with an increase in levels of phosphorylated Akt, an indicator of phosphoinositide 3-kinase (PI3K) activity, and decreased nuclear histone deacetylase (HDAC)2 levels. Treatment with an miR-21¿specific antagomir (Ant-21) increased phosphatase and tensin homolog levels. Treatment with Ant-21, or the pan-PI3K inhibitor LY294002, reduced PI3K activity and restored HDAC2 levels. This led to suppression of airway hyperresponsiveness and restored steroid sensitivity to allergic airway disease. These observations were replicated with SSIAAD associated with 4 different pathogens. Conclusion We identify a previously unrecognized role for an¿miR-21/PI3K/HDAC2 axis in SSIAAD. Our data highlight miR-21 as a novel therapeutic target for the treatment of this form of asthma.

DOI 10.1016/j.jaci.2016.04.038
Citations Scopus - 28Web of Science - 28
Co-authors Joerg Mattes, Jay Horvat, Paul Foster, Malcolm Starkey, Philip Hansbro, Simon Keely
2017 Liu G, Cooley MA, Nair PM, Donovan C, Hsu AC, Jarnicki AG, et al., 'Airway remodelling and inflammation in asthma are dependent on the extracellular matrix protein fibulin-1c', JOURNAL OF PATHOLOGY, 243 510-523 (2017) [C1]
DOI 10.1002/path.4979
Citations Scopus - 5Web of Science - 5
Co-authors Christopher Grainge, Philip Hansbro, Peter Wark, Darryl Knight, Paul Foster, Jay Horvat, Alan Hsu, Gang Liu, Hock Tay, Chantal Donovan
2017 Dua K, Hansbro NG, Foster PS, Hansbro PM, 'MicroRNAs as therapeutics for future drug delivery systems in treatment of lung diseases', Drug Delivery and Translational Research, 7 168-178 (2017) [C1]

© 2016, Controlled Release Society. The rapid advancement in the area of microRNAs (miRNAs) from discovery to their translation into therapeutic moieties reflects their significan... [more]

© 2016, Controlled Release Society. The rapid advancement in the area of microRNAs (miRNAs) from discovery to their translation into therapeutic moieties reflects their significance as important regulators in the management of disease pathology. The miRNAs can potentially be a new class of drugs in the near future for the treatment of various lung diseases, but it lacks the current knowledge how these identified therapeutic moieties can be designed into an effective, patient complaint and targeted drug delivery system. miRNAs have characteristic features like small size and low molecular weight which makes them easily translated into an effective drug delivery system. In this review, we have summarised the concept of miRNAs and different approaches which can be employed to deliver miRNAs effectively and safely to the target cells including the challenges associated with their development in particular emphasis on pulmonary diseases. Such approaches will be of interest for both the biological and formulation scientists to understand and explore the new vistas in the area of miRNA delivery for pulmonary inflammatory diseases.

DOI 10.1007/s13346-016-0343-6
Citations Scopus - 13Web of Science - 12
Co-authors Paul Foster, Philip Hansbro
2017 Kim RY, Pinkerton JW, Essilfie AT, Robertson AAB, Baines KJ, Brown AC, et al., 'Role for NLRP3 inflammasome-mediated, IL-1ß-dependent responses in severe, steroid-resistant asthma', American Journal of Respiratory and Critical Care Medicine, 196 283-297 (2017) [C1]

© 2017 by the American Thoracic Society. Rationale: Severe, steroid-resistant asthma is the major unmet need in asthma therapy. Disease heterogeneity and poor understanding of pat... [more]

© 2017 by the American Thoracic Society. Rationale: Severe, steroid-resistant asthma is the major unmet need in asthma therapy. Disease heterogeneity and poor understanding of pathogenic mechanisms hampers the identification of therapeutic targets. Excessive nucleotide-binding oligomerization domain-like receptor family, pyrin domain-containing 3 (NLRP3) inflammasome and concomitant IL-1ß responses occur in chronic obstructive pulmonary disease, respiratory infections, and neutrophilic asthma. However, the direct contributions to pathogenesis, mechanisms involved, and potential for therapeutic targeting remain poorly understood, and are unknown in severe, steroid-resistant asthma. Objectives: To investigate the roles and therapeutic targeting of the NLRP3 inflammasome and IL-1ß in severe, steroid-resistant asthma. Methods: We developed mouse models of Chlamydia and Haemophilus respiratory infection-mediated, ovalbumin-induced severe, steroid-resistant allergic airway disease. These models share the hallmark features of human disease, including elevated airway neutrophils, and NLRP3 inflammasome and IL-1ß responses. The roles and potential for targeting of NLRP3 inflammasome, caspase-1, and IL-1ß responses in experimental severe, steroid-resistant asthma were examined using a highly selective NLRP3 inhibitor, MCC950; the specific caspase-1 inhibitor Ac-YVAD-cho; and neutralizing anti-IL-1ß antibody. Roles for IL-1ß-induced neutrophilic inflammation were examined using IL-1ß and anti-Ly6G. Measurements and Main Results: Chlamydia and Haemophilus infections increase NLRP3, caspase-1, IL-1ß responses that drive steroid-resistant neutrophilic inflammation and airway hyperresponsiveness. Neutrophilic airway inflammation, disease severity, and steroid resistance in human asthma correlate with NLRP3 and IL-1ß expression. Treatment with anti-IL-1ß, Ac- YVAD-cho, and MCC950 suppressed IL-1ß responses and the important steroid-resistant features of disease in mice, whereas IL-1ß administration recapitulated these features. Neutrophil depletion suppressed IL-1ß-induced steroid-resistant airway hyperresponsiveness. Conclusions: NLRP3 inflammasome responses drive experimental severe, steroid-resistant asthma and are potential therapeutic targets in this disease.

DOI 10.1164/rccm.201609-1830OC
Citations Scopus - 26Web of Science - 22
Co-authors Darryl Knight, Jay Horvat, Lisa Wood, Katherine Baines, Malcolm Starkey, Jodie Simpson, Peter Gibson, Philip Hansbro, Peter Wark
2016 Thorburn AN, Tseng H-Y, Donovan C, Hansbro NG, Jarnicki AG, Foster PS, et al., 'TLR2, TLR4 AND MyD88 Mediate Allergic Airway Disease (AAD) and Streptococcus pneumoniae-Induced Suppression of AAD.', PLoS One, 11 e0156402 (2016) [C1]
DOI 10.1371/journal.pone.0156402
Citations Scopus - 6Web of Science - 4
Co-authors Paul Foster, Peter Gibson, Philip Hansbro, Chantal Donovan
2014 Maltby S, Hansbro NG, Tay HL, Stewart J, Plank M, Donges B, et al., 'Production and differentiation of myeloid cells driven by proinflammatory cytokines in response to acute pneumovirus infection in mice.', J Immunol, 193 4072-4082 (2014) [C1]
DOI 10.4049/jimmunol.1400669
Citations Scopus - 12Web of Science - 11
Co-authors Steven Maltby, Hock Tay, Paul Foster
2014 Grafton KT, Moir LM, Black JL, Hansbro NG, Hansbro PM, Burgess JK, Oliver BG, 'LF-15 & T7, synthetic peptides derived from tumstatin, attenuate aspects of airway remodelling in a murine model of chronic OVA-induced allergic airway disease', PLoS ONE, 9 (2014) [C1]

Background: Tumstatin is a segment of the collagen-IV protein that is markedly reduced in the airways of asthmatics. Tumstatin can play an important role in the development of air... [more]

Background: Tumstatin is a segment of the collagen-IV protein that is markedly reduced in the airways of asthmatics. Tumstatin can play an important role in the development of airway remodelling associated with asthma due to its antiangiogenic properties. This study assessed the anti-angiogenic properties of smaller peptides derived from tumstatin, which contain the interface tumstatin uses to interact with the aVb3 integrin. Methods: Primary human lung endothelial cells were exposed to the LF-15, T3 and T7 tumstatin-derived peptides and assessed for cell viability and tube formation in vitro. The impact of the anti-angiogenic properties on airways hyperresponsiveness (AHR) was then examined using a murine model of chronic OVA-induced allergic airways disease. Results: The LF-15 and T7 peptides significantly reduced endothelial cell viability and attenuated tube formation in vitro. Mice exposed to OVA+ LF-15 or OVA+T7 also had reduced total lung vascularity and AHR was attenuated compared to mice exposed to OVA alone. T3 peptides reduced cell viability but had no effect on any other parameters. Conclusion: The LF-15 and T7 peptides may be appropriate candidates for use as novel pharmacotherapies due to their small size and anti-angiogenic properties observed in vitro and in vivo. © 2014 Grafton et al.

DOI 10.1371/journal.pone.0085655
Citations Scopus - 4Web of Science - 4
Co-authors Philip Hansbro
2013 Eftekhari P, Hajizadeh S, Reza Raoufy M, Reza Masjedi M, Yang M, Hansbro N, et al., 'Preventive effect of N-acetylcysteine in a mouse model of steroid resistant acute exacerbation of asthma', EXCLI Journal, 12 184-192 (2013) [C1]

Oxidative stress appears to have an important role in glucocorticoid insensitivity, as a crucial problem in asthma therapy. We studied the preventive effect of antioxidant N-acety... [more]

Oxidative stress appears to have an important role in glucocorticoid insensitivity, as a crucial problem in asthma therapy. We studied the preventive effect of antioxidant N-acetylcysteine (NAC) on the airway hyper-responsiveness (AHR) and the accumulation of inflammatory cells in the airways in an animal model of steroid resistant acute exacerbation of asthma. Systemically sensitized Balb/C mice were exposed to Ovalbumin aerosol on days 13, 14, 15 and 16, followed by intratracheal lipopolysaccharide (LPS) to induce acute exacerbation. NAC (intraperitoneal, 320 mg/kg 30 min before and 12 hours after each challenge) reduced hyperresponsiveness with/out dexamethasone. LPS application caused neutrophilia in bronchoalveolar lavage fluid (BALF) and eosinophil count was higher than respective control in BALF as well as neutrophils after dexamethasone treatment. NAC significantly decreased neutrophil and eosinophil count in BALF as well as inflammatory cytokines (IL-13 and IL-5).We concluded that addition of NAC to asthma therapy has beneficial preventive effects in an animal model of steroid resistant acute exacerbation of asthma.

Citations Scopus - 4Web of Science - 3
Co-authors Paul Foster, Ming Yang
2013 Beckett EL, Stevens RL, Jarnicki AG, Kim RY, Hanish I, Hansbro NG, et al., 'A new short-term mouse model of chronic obstructive pulmonary disease identifies a role for mast cell tryptase in pathogenesis', The Journal of Allergy and Clinical Immunology, 131 752-762 (2013) [C1]
Citations Scopus - 98Web of Science - 98
Co-authors Peter Wark, Emma Beckett, Jay Horvat, Ming Yang, Philip Hansbro, Simon Keely, Paul Foster
2013 Simpson JL, McDonald VM, Baines KJ, Oreo KM, Wang F, Hansbro PM, Gibson PG, 'Influence of Age, Past Smoking, and Disease Severity on TLR2, Neutrophilic Inflammation, and MMP-9 Levels in COPD', MEDIATORS OF INFLAMMATION, (2013) [C1]
DOI 10.1155/2013/462934
Citations Scopus - 23Web of Science - 18
Co-authors Katherine Baines, Jodie Simpson, Vanessa Mcdonald, Philip Hansbro, Peter Gibson
2013 Collison A, Siegle JS, Hansbro NG, Kwok C-T, Herbert C, Mattes J, et al., 'Epigenetic changes associated with disease progression in a mouse model of childhood allergic asthma', DISEASE MODELS & MECHANISMS, 6 993-1000 (2013) [C1]
DOI 10.1242/dmm.011247
Citations Scopus - 13Web of Science - 12
Co-authors Adam Collison, Joerg Mattes, Paul Foster
2013 Herbert C, Siegle JS, Shadie AM, Nikolaysen S, Garthwaite L, Hansbro NG, et al., 'Development of asthmatic inflammation in mice following early-life exposure to ambient environmental particulates and chronic allergen challenge', DMM Disease Models and Mechanisms, 6 479-488 (2013) [C1]
Citations Scopus - 13Web of Science - 14
Co-authors Paul Foster
2011 Siegle JS, Hansbro NG, Dong C, Angkasekwinai P, Foster PS, Kumar RK, 'Blocking induction of T helper type 2 responses prevents development of disease in a model of childhood asthma', Clinical and Experimental Immunology, 165 19-28 (2011) [C1]
DOI 10.1111/j.1365-2249.2011.04392.x
Citations Scopus - 28Web of Science - 28
Co-authors Paul Foster
2011 Davidson SK, Kaiko GE, Loh Z, Lalwani A, Zhang V, Spann K, et al., 'Plasmacytoid Dendritic Cells promote host defense against Acute Pneumovirus infection via the TLR7-MyD88-Dependent signaling pathway', Journal of Immunology, 186 5938-5948 (2011) [C1]
DOI 10.4049/jimmunol.1002635
Citations Scopus - 56Web of Science - 53
Co-authors Paul Foster, Gerard Kaiko
2010 Lau JY, Oliver BG, Baraket M, Beckett EL, Hansbro NG, Moir LM, et al., 'Fibulin-1 Is increased in asthma - A novel mediator of airway remodeling?', Plos One, 5 1-13 (2010) [C1]
DOI 10.1371/journal.pone.0013360
Citations Scopus - 29Web of Science - 28
Co-authors Emma Beckett, Philip Hansbro, Paul Foster
2010 Burgess JK, Boustany S, Moir LM, Weckmann M, Lau JY, Grafton K, et al., 'Reduction of tumstatin in asthmatic airways contributes to angiogenesis, inflammation, and hyperresponsiveness', American Journal of Respiratory and Critical Care Medicine, 181 106-115 (2010) [C1]
DOI 10.1164/rccm.200904-0631oc
Citations Scopus - 40Web of Science - 37
Co-authors Paul Foster, Philip Hansbro
2010 Siegle JS, Hansbro NG, Herbert C, Rosenberg HF, Domachowske JB, Asquith KL, et al., 'Early-life viral infection and allergen exposure interact to induce an asthmatic phenotype in mice', Respiratory Research, 11 1-15 (2010) [C1]
DOI 10.1186/1465-9921-11-14
Citations Scopus - 57Web of Science - 54
Co-authors Paul Foster, Kelly Asquith
2009 Phipps S, Hansbro NG, Lam CE, Foo A, Matthaei KI, Foster PS, 'Allergic sensitization is enhanced in early life through toll-like receptor 7 activation', Clinical and Experimental Allergy, 39 1920-1928 (2009) [C1]
DOI 10.1111/j.1365-2222.2009.03335.x
Citations Scopus - 11Web of Science - 11
Co-authors Paul Foster
2008 Ito K, Herbert C, Siegle JS, Vuppusetty C, Hansbro NG, Thomas PS, et al., 'Steroid-resistant neutrophilic inflammation in a mouse model of an acute exacerbation of asthma', American Journal of Respiratory Cell and Molecular Biology, 39 543-550 (2008) [C1]
DOI 10.1165/rcmb.2008-0028oc
Citations Scopus - 84Web of Science - 77
Co-authors Paul Foster
2008 Su Y-C, Rolph MS, Hansbro NG, Mackay CR, Sewell WA, 'Granulocyte-macrophage colony-stimulating factor is required for bronchial eosinophilia in a murine model of allergic airway inflammation', Journal of Immunology, 180 2600-2607 (2008) [C1]
Citations Scopus - 30Web of Science - 29
2008 Hansbro NG, Horvat JC, Wark PA, Hansbro PM, 'Understanding the mechanisms of viral induced asthma: New therapeutic directions', Pharmacology & Therapeutics, 117 313-353 (2008) [C1]
DOI 10.1016/j.pharmthera.2007.11.002
Citations Scopus - 76Web of Science - 71
Co-authors Jay Horvat, Peter Wark, Philip Hansbro
2007 Horvat JC, Beagley KW, Wade MA, Preston JA, Hansbro NG, Hickey DK, et al., 'Neonatal chlamydial infection induces mixed T-cell responses that drive allergic airway disease', American Journal of Respiratory and Critical Care Medicine, 176 556-564 (2007) [C1]
DOI 10.1164/rccm.200607-1005OC
Citations Scopus - 66Web of Science - 65
Co-authors Jay Horvat, Philip Hansbro, Paul Foster, Gerard Kaiko, Peter Gibson
2007 Weckmann M, Collison A, Simpson JL, Kopp MV, Wark PA, Smyth MJ, et al., 'Critical link between TRAIL and CCL20 for the activation of T(H)2 cells and the expression of allergic airway disease', Nature Medicine, 13 1308-1315 (2007) [C1]
DOI 10.1038/nm1660
Citations Scopus - 82Web of Science - 81
Co-authors Peter Gibson, Jodie Simpson, Peter Wark, Adam Collison, Paul Foster, Joerg Mattes
2006 Siegle JS, Hansbro NG, Herbert C, Yang M, Foster PS, Kumar RK, 'Airway hyperreactivity in exacerbation of chronic asthma is independent of elosinophilic inflammation', American Journal of Respiratory Cell and Molecular Biology, 35 565-570 (2006) [C1]
DOI 10.1165/rcmb.2006-0135OC
Citations Scopus - 46Web of Science - 43
Co-authors Paul Foster, Ming Yang
2004 Hansbro NG, Beagley LG, Christiansen D, Loveland BE, Johansson ES, Beagley KW, et al., 'Novel role for decay-accelerating factor in Coxsackievirus A21-mediated cell infectivity', Journal of Virology, 78 12677-12682 (2004) [C1]
DOI 10.1128/JVI.78.22.12677-12682.2004
Citations Scopus - 5Web of Science - 5
2004 Hansbro NG, Johansson ES, Au GG, Lindberg A, Barry RD, Shafren DR, 'Enterovirus capsid interactions with decay-accelerating factor mediate lytic cell infection', Journal of Virology, 78 1431-1439 (2004) [C1]
DOI 10.1128/JVI.78.3.1431-1439.2004
Citations Scopus - 7Web of Science - 6
Co-authors Gough Au
2004 Shafren DR, Au GG, Nguyen T, Barry RD, Hansbro NG, Harvey ES, et al., 'Systemic therapy of malignant human melanoma tumors by a common cold-producing enterovirus, Coxsackievirus A21', Clinical Cancer Research, 10 53-60 (2004) [C1]
DOI 10.1158/1078-0432.CCR-0690-3
Citations Scopus - 66Web of Science - 70
Co-authors Gough Au, Erin Harvey
2000 Hansbro NG, Clulow J, Man SY, Jones RC, 'pH and bicarbonate in the ductuli efferentes testis of the rat', INTERNATIONAL JOURNAL OF ANDROLOGY, 23 46-50 (2000) [C1]
Citations Scopus - 10Web of Science - 10
Co-authors John Clulow
Show 34 more journal articles

Conference (24 outputs)

Year Citation Altmetrics Link
2016 Brown AC, Essilfie AT, Beckett EL, Thorburn AN, Hansbro NG, Jarnicki AG, et al., 'The role of CD8 T-cells during anti-PD1 treatment of viral infection-induced secondary bacterial pneumonia', EUROPEAN JOURNAL OF IMMUNOLOGY, Melbourne, AUSTRALIA (2016)
Co-authors Paul Foster, Jay Horvat, Peter Wark, Philip Hansbro
2013 Kumar RK, Collison A, Siegle JS, Hansbro NG, Kwok C-T, Herbert C, et al., 'Epigenetic Changes Associated With Disease Progression In A Model Of Childhood Allergic Asthma', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE (2013)
Co-authors Adam Collison, Paul Foster, Joerg Mattes
2013 Hansbro P, Beckett E, Stevens R, Jarnicki A, Kim R, Hanish I, et al., 'A short-term model of COPD identifies a role for mast cell tryptase', JOURNAL OF IMMUNOLOGY, Honolulu, HI (2013) [E3]
Co-authors Paul Foster, Simon Keely, Philip Hansbro, Ming Yang, Jay Horvat, Peter Wark, Emma Beckett
2013 Herbert C, Siegle JS, Shadie AM, Nikolaysen S, Garthwaite L, Hansbro NG, et al., 'EARLY LIFE EXPOSURE TO ENVIRONMENTAL PARTICULATES PREDISPOSES TO DEVELOPMENT OF ASTHMATIC INFLAMMATION', RESPIROLOGY (2013) [E3]
Co-authors Paul Foster
2010 Ptaschinski CM, Phipps S, Hansbro NG, Rosenberg HF, Mattes J, Foster PS, 'MicroRNAs are involved in the regulation of inflammatory responses characteristic of severe respiratory virus infection', American Journal of Respiratory and Critical Care Medicine, New Orleans (2010) [E3]
Co-authors Joerg Mattes, Paul Foster
2010 Siegle J, Hansbro NG, Dong C, Angkasekwinai P, Foster PS, Kumar R, 'Anti-Th2 cytokines inhibit progression in a murine model of childhood asthma', European Respiratory Society Annual Congress 2010. Abstracts, Barcelona, Spain (2010) [E3]
Co-authors Paul Foster
2009 Herbert C, Scruton K, Hsu K, Siegle JS, Hansbro NG, Foster PS, et al., 'Enhanced expression of cytokines by pulmonary T-cells and macrophages in a model of exacerbations of chronic asthma', American Journal of Respiratory and Critical Care Medicine, San Diego, CA (2009) [E3]
Co-authors Paul Foster
2009 Siegle JS, Hansbro NG, Herbert C, Rosenberg HF, Asquith KL, Foster PS, Kumar RK, 'Interaction between early-life viral infection and allergen exposure induces an asthmatic phenotype in mice', Respirology, Darwin, NT (2009) [E3]
DOI 10.1111/j.1440-1843.2009.01502_7.x
Co-authors Paul Foster, Kelly Asquith
2009 Weckmann M, Lau J, Grafton K, Oliver B, Hansbro NG, Foster PS, et al., 'Tumstatin: A non-collagenous domain of collagen IV: Effects on inflammation and angiogenesis', Respirology, Darwin, NT (2009) [E3]
Co-authors Philip Hansbro, Paul Foster
2009 Schilter HC, Shum B, Shim D, Maslowski K, Tsai L, Kim R, et al., 'Fatty acid binding proteins: A link between metabolism and airway inflammation?', Respirology, Darwin, NT (2009) [E3]
Co-authors Philip Hansbro
2008 Burgess JK, Boustany S, Oliver BG, Moir LM, Baraket M, Hansbro PM, et al., 'The absence of tumstatin in asthma may lead to angiogenesis and airway hyperresponsiveness', American Journal of Respiratory and Critical Care Medicine, Toronto, ONT (2008) [E3]
Co-authors Philip Hansbro, Paul Foster
2008 Hansbro NG, Boustany S, Oliver B, Burgess J, Black J, Rosenberg H, et al., 'Early life pneumoviral infection induces the development of pulmonary angiogenesis', Respirology, Melbourne, VIC (2008) [E3]
DOI 10.1111/j.1440-1843.2008.01252.x
Co-authors Philip Hansbro, Paul Foster
2008 Boustany S, Oliver BG, Moir LM, Black JL, Hansbro PM, Hansbro NG, et al., 'Tumstatin, an angiogenic inhibitor, modulates airway angiogenesis', Respirology, Melbourne, VIC (2008) [E3]
DOI 10.1111/j.1440-1843.2008.01252_4.x
Co-authors Philip Hansbro, Paul Foster
2008 Schilter H, Shim D, Maslowski K, Tsai L, Shum B, Kim RY, et al., 'A role for fatty acid binding proteins in respiratory inflammation', Australasian Society for Immunology 38th Annual Scientific Meeting: Delegate Book, Canberra, ACT (2008) [E3]
Co-authors Philip Hansbro
2007 Horvat JC, Garside CG, Wade MA, Preston JA, Hansbro NG, Gibson PG, et al., 'Development of allergic airways disease is differentially affected by chlamydial respiratory infection at different ages', American Journal of Respiratory and Critical Care Medicine, San Francisco, Calif. (2007) [E3]
Co-authors Philip Hansbro, Paul Foster, Jay Horvat, Peter Gibson
2007 Grissell TV, Hansbro NG, Hsu A, Mimica J, Wark PA, 'Response of primary bronchoepithelial cells from COPD, asthmatic and healthy subjects to infection with avian and human influenza virus strains', Respirology (Abstracts of the 12th Congress of the Asian Pacific Society of Respirology), Gold Coast, QLD (2007) [E3]
Co-authors Peter Wark
2007 Hansbro NG, Boustany S, Oliver BG, Burgess JK, Black JL, Hansbro PM, Foster PS, 'Viral-induced angiogenesis', Immuno 2007: 13th International Congress of Immunology. Abstracts and Posters, Rio de Janeiro, Brazil (2007) [E3]
Co-authors Philip Hansbro, Paul Foster
2007 Horvat JC, Moller CG, Wade MA, Preston JA, Hansbro NG, Gibson PG, et al., 'Allergic airways disease (AAD) is differentially affected by chlamydial lung infection at different stages of life', Respirology (TSANZ Abstracts-Posters), Auckland (2007) [E3]
DOI 10.1111/j.1440-1843.2007.001050.x
Co-authors Philip Hansbro, Jay Horvat, Paul Foster, Peter Gibson
2006 Kaiko GE, Phipps S, Lam CE, Hickey DK, Hansbro NG, Foster PS, Beagley KW, 'The chlamydia infection of dendritic cells drives the development of a pro-asthmatic response', Immunology and Cell Biology, Auckland, NZ (2006) [E3]
Co-authors Paul Foster, Gerard Kaiko
2006 Horvat JC, Moller CG, Wade MA, Preston JA, Hansbro NG, Gibson PG, et al., 'The development of allergic airways disease (AAD) is differently affected by chlamydial lung infection at different stages of life', Immunology and Cell Biology, Auckland, NZ (2006) [E3]
Co-authors Jay Horvat, Peter Gibson, Paul Foster, Philip Hansbro
2006 Horvat JC, Wade MA, Preston JA, Hansbro NG, Gibson PG, Beagley KW, et al., 'Early life chlamydial lung infection enhances allergic airways disease (AAD)', Respirology, Canberra (2006) [E3]
Co-authors Paul Foster, Jay Horvat, Peter Gibson, Philip Hansbro
2006 Horvat JC, Wade MA, Preston JA, Hansbro NG, Gibson PG, Beagley KW, et al., 'Neonatal chlamydial infection exacerbates allergic airways disease', Abstracts ATS 2006 International Conference, San Diego, California (2006) [E3]
Co-authors Peter Gibson, Philip Hansbro, Jay Horvat, Paul Foster
2005 Horvat JC, Preston JA, Hansbro NG, Ferguson AL, Gibson PG, Beagley KW, et al., 'Neonatal chlamydial infection inhibits the development of allergic airway inflammation in adult mice', Inflammation Research, Melbourne, Australia (2005) [E3]
Co-authors Jay Horvat, Philip Hansbro, Paul Foster, Peter Gibson
2003 Jones RC, Knee RA, Ecroyd HW, Hansbro NG, Clulow J, Aitken RJ, Beagley KW, 'Delivery of Antibodies for Male Immunocontraception', The Third International Conference on the Epididymis, Charlottesville, Virginia (2003) [E3]
Co-authors John Aitken, John Clulow
Show 21 more conferences
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Grants and Funding

Summary

Number of grants 13
Total funding $568,574

Click on a grant title below to expand the full details for that specific grant.


20173 grants / $200,000

Asthma treatments$120,000

Funding body: AstraZeneca

Funding body AstraZeneca
Project Team Professor Phil Hansbro, Doctor Nicole Hansbro, Associate Professor Jay Horvat
Scheme Research Grant
Role Investigator
Funding Start 2017
Funding Finish 2017
GNo G1700098
Type Of Funding C3211 - International For profit
Category 3211
UON Y

MD990 and murine smoking model$40,000

Funding body: AusBio Limited

Funding body AusBio Limited
Project Team Professor Phil Hansbro, Doctor Nicole Hansbro
Scheme Entrepreneurs' Programme: Innovation Connections
Role Investigator
Funding Start 2017
Funding Finish 2017
GNo G1700108
Type Of Funding C3111 - Aust For profit
Category 3111
UON Y

MD990 and murine smoking model$40,000

Funding body: Department of Industry, Innovation and Science

Funding body Department of Industry, Innovation and Science
Project Team Professor Phil Hansbro, Doctor Nicole Hansbro
Scheme Entrepreneurs' Programme: Innovation Connections
Role Investigator
Funding Start 2017
Funding Finish 2017
GNo G1701037
Type Of Funding Other Public Sector - Commonwealth
Category 2OPC
UON Y

20162 grants / $116,724

COPD treatments$68,724

Funding body: PharmAkea Inc

Funding body PharmAkea Inc
Project Team Professor Phil Hansbro, Doctor Nicole Hansbro
Scheme Research Project
Role Investigator
Funding Start 2016
Funding Finish 2016
GNo G1601160
Type Of Funding C3211 - International For profit
Category 3211
UON Y

MD990 Respiratory Project$48,000

Funding body: AusBio Limited

Funding body AusBio Limited
Project Team Professor Phil Hansbro, Doctor Nicole Hansbro
Scheme Research Project
Role Investigator
Funding Start 2016
Funding Finish 2016
GNo G1600515
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON Y

20131 grants / $20,000

DP73 Digital colour and monochrome camera + cellSens software + Xcite120 fluorescence lamp illuminator$20,000

Funding body: NHMRC (National Health & Medical Research Council)

Funding body NHMRC (National Health & Medical Research Council)
Project Team Laureate Professor Paul Foster, Doctor Alan Hsu, Professor Phil Hansbro, Professor Joerg Mattes, Doctor Katie Baines, Professor Jodie Simpson, Professor Rakesh Kumar, Doctor Nicole Hansbro, Doctor Steven Maltby, Doctor Ming Yang, Doctor Gerard Kaiko, Associate Professor Jay Horvat, Associate Professor Simon Keely, Doctor Andrew Jarnicki, Doctor Michael Fricker
Scheme Equipment Grant
Role Investigator
Funding Start 2013
Funding Finish 2013
GNo G1201186
Type Of Funding Other Public Sector - Commonwealth
Category 2OPC
UON Y

20121 grants / $50,000

SpectraMax M5e Multi-Mode Microplate Reader$50,000

Funding body: NHMRC (National Health & Medical Research Council)

Funding body NHMRC (National Health & Medical Research Council)
Project Team Laureate Professor Paul Foster, Professor Phil Hansbro, Professor Joerg Mattes, Professor Rakesh Kumar, Doctor Nicole Hansbro, Doctor Ming Yang, Associate Professor Jay Horvat, Associate Professor Simon Keely, Doctor Andrew Jarnicki, Doctor Linda Howland, Doctor Kelly Asquith
Scheme Equipment Grant
Role Investigator
Funding Start 2012
Funding Finish 2012
GNo G1100975
Type Of Funding Other Public Sector - Commonwealth
Category 2OPC
UON Y

20111 grants / $45,000

SCIREQ FlexiVentFX system + FlexiVentFX extension$45,000

Funding body: NHMRC (National Health & Medical Research Council)

Funding body NHMRC (National Health & Medical Research Council)
Project Team Professor Phil Hansbro, Laureate Professor Paul Foster, Professor Joerg Mattes, Associate Professor Simon Keely, Associate Professor Jay Horvat, Doctor Nicole Hansbro, Doctor Ming Yang, Doctor Catherine Ptaschinski, Doctor Kelly Asquith, Doctor Gough Au, Conjoint Professor Peter Wark, Laureate Professor John Aitken, Conjoint Professor Keith Jones, Laureate Professor Roger Smith, Professor Judith Black, Professor Rakesh Kumar, Professor Paul Hertzog
Scheme Equipment Grant
Role Investigator
Funding Start 2011
Funding Finish 2011
GNo G1100037
Type Of Funding Other Public Sector - Commonwealth
Category 2OPC
UON Y

20101 grants / $39,000

Buxco FinePointe software and FinePointe RC system for mice $39,000

Funding body: NHMRC (National Health & Medical Research Council)

Funding body NHMRC (National Health & Medical Research Council)
Project Team Laureate Professor Paul Foster, Professor Phil Hansbro, Professor Joerg Mattes, Doctor Nicole Hansbro, Doctor Simon Phipps, Doctor Ming Yang, Doctor Kelly Asquith, Doctor Catherine Ptaschinski, Professor Rakesh Kumar, Professor Judith Black
Scheme Equipment Grant
Role Investigator
Funding Start 2010
Funding Finish 2010
GNo G1000053
Type Of Funding Other Public Sector - Commonwealth
Category 2OPC
UON Y

20091 grants / $41,150

Coulter counter$41,150

Funding body: NHMRC (National Health & Medical Research Council)

Funding body NHMRC (National Health & Medical Research Council)
Project Team Laureate Professor Paul Foster, Professor Phil Hansbro, Professor Joerg Mattes, Doctor Simon Phipps, Doctor Ming Yang, Doctor Nicole Hansbro, Doctor Kelly Asquith
Scheme Equipment Grant
Role Investigator
Funding Start 2009
Funding Finish 2009
GNo G0189851
Type Of Funding Other Public Sector - Commonwealth
Category 2OPC
UON Y

20081 grants / $35,000

Individually ventilated cages (IVC) and associated ventilator, holding boxes and water bottles$35,000

Funding body: NHMRC (National Health & Medical Research Council)

Funding body NHMRC (National Health & Medical Research Council)
Project Team Laureate Professor Paul Foster, Professor Phil Hansbro, Professor Joerg Mattes, Doctor Simon Phipps, Doctor Ming Yang, Doctor Nicole Hansbro, Doctor Kelly Asquith
Scheme Equipment Grant
Role Investigator
Funding Start 2008
Funding Finish 2008
GNo G0188541
Type Of Funding Other Public Sector - Commonwealth
Category 2OPC
UON Y

20072 grants / $21,700

The role of tumstatin in angiogenesis and asthma$20,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Laureate Professor Paul Foster, Doctor Nicole Hansbro, Doctor Simon Phipps, Professor Phil Hansbro
Scheme Project Grant
Role Investigator
Funding Start 2007
Funding Finish 2007
GNo G0187238
Type Of Funding Contract - Aust Non Government
Category 3AFC
UON Y

The 13th International COngress of Immunology, Rio de Janeoro, Brazil, 21/8/2007 - 25/8/2007$1,700

Funding body: University of Newcastle

Funding body University of Newcastle
Project Team Doctor Nicole Hansbro
Scheme Travel Grant
Role Lead
Funding Start 2007
Funding Finish 2007
GNo G0188062
Type Of Funding Internal
Category INTE
UON Y
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Dr Nicole Hansbro

Position

Conjoint Fellow
Asthma, Allergy and Inflammation Research Centre
School of Biomedical Sciences and Pharmacy
Faculty of Health and Medicine

Focus area

Immunology and Microbiology

Contact Details

Email nicole.hansbro@newcastle.edu.au
Phone (02) 40420164
Fax (02) 40420024

Office

Room HMRI 2403
Building Hunter Medical Research Institute
Location Hunter Medical Research Institute

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