Dr Punnam Chander Veerati

Dr Punnam Chander Veerati

Postdoctoral Researcher

School of Medicine and Public Health

Career Summary

Biography

Punnam Chander completed Bachelors of Pharmacy in 2009 with a first-class distinction at an average of 80.7% and stood 6th rank in the University. He was awarded a fellowship from All India Council for Technical Education (AITEC) after qualifying GATE exam with 92.28 percentile to pursue Masters of Pharmacy. He opted Pharmacology as a specialization in Masters and completed in 2011 with a first-class distinction (76.5%). Later, he worked as a Research Associate in Invivo Pharmacology R&D department at Glenmark Pharmaceuticals Ltd for approximately four years, where he screened various potential drug candidates (new chemical entities) for asthma, COPD, diabetes, rheumatoid arthritis and neuropathic pain in animal models. In 2015, he was awarded University Postgraduate Research Fellowship to pursue higher research degree (PhD) in the University of Newcastle, Australia. He moved to Newcastle and joined Dr Grainge’s team to investigate the role of mechanical forces on asthma pathogenesis. He presented his data in various national and international conferences and also aided in providing compelling data for a successful NHMRC grant. He was awarded PhD in July 2019 and now working as a postdoctoral researcher in the same lab. 


Qualifications

  • Doctor of Philosophy in Medicine, University of Newcastle
  • Bachelor of Pharmacy, Kakatiya University, India
  • Master of Pharmacy, Kakatiya University, India

Keywords

  • Air-liquid interface (ALI) culture
  • Animal models
  • Asthma
  • Bronchoconstriction
  • COPD
  • Compressive stress
  • ELISA
  • In-vitro
  • Innate immunity
  • Mechanical forces
  • Molecular biology techniques
  • Pharmacology
  • Primary bronchial epithelial cells
  • RP-HPLC
  • Respiratory
  • Rhinovirus
  • Shear stress
  • Size exclusion chromatography
  • Toxicology
  • qPCR

Languages

  • Telugu (Mother)
  • English (Fluent)
  • Hindi (Fluent)

Fields of Research

Code Description Percentage
110203 Respiratory Diseases 100

Professional Experience

UON Appointment

Title Organisation / Department
Postdoctoral Researcher University of Newcastle
School of Medicine and Public Health
Australia
Postdoctoral Researcher Priority Research Centre (PRC) for Healthy Lungs | The University of Newcastle
School of Medicine and Public Health
Australia
Postdoctoral Researcher University of Newcastle
School of Medicine and Public Health
Australia

Academic appointment

Dates Title Organisation / Department
3/12/2018 - 9/7/2019 Postdoctoral Researcher School of Medicine & Public Health, Faculty of Health & Medicine, University of Newcastle | Australia
Australia

Professional appointment

Dates Title Organisation / Department
16/2/2018 - 31/12/2018 Casual Research Assistant

Performed ELISAs and other assays to measure snake venom from blood obtained from envenomed people. Isolated toxins fractions from different Australian snake venom samples using RP-HPLC and size exclusion chromatography techniques.  

School of Medicine & Public Health, Faculty of Health & Medicine, University of Newcastle | Australia
Clinical Toxicology Research Group
Australia
18/7/2011 - 30/4/2015 Research Associate

I was a member of In-vivo Pharmacology team at Glenmark. I was involved in designing, planning, and execution of experiments, data compilation, interpretation and report generation. I worked on different in-vivo disease models of Asthma, COPD, Allergic Rhinitis, Rheumatoid Arthritis, Neuropathic pain, and Diabetes.  

Glenmark Pharmaceuticals Ltd
In-vivo Pharmacology
India
5/1/2018 - 30/3/2018 Casual Laboratory Assistant

Prepared Australian Lung Biobank kits 

Priority Research Centre (PRC) for Healthy Lungs | The University of Newcastle
Australia
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Publications

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


Chapter (1 outputs)

Year Citation Altmetrics Link
2019 Reid AT, Sutanto EN, Chander-Veerati P, Looi K, Li NF, Iosifidis T, et al., 'Ground zero-the airway epithelium', Rhinovirus Infections: Rethinking the Impact on Human Health and Disease, Academic Press, Cambridge, MS 61-98 (2019) [B1]
DOI 10.1016/B978-0-12-816417-4.00003-2
Co-authors Andrew Reid

Journal article (10 outputs)

Year Citation Altmetrics Link
2020 Tasoulis T, Silva A, Veerati P, Dunstan N, Baker M, Hodgson W, Isbister G, 'INTRA-SPECIFIC VENOM VARIATION IN COASTAL TAIPANS', TOXICON, 177 S42-S42 (2020)
Co-authors Mark Baker, Geoffrey Isbister
2020 Kicic A, de Jong E, Ling K-M, Nichol K, Anderson D, Wark PAB, et al., 'Assessing the unified airway hypothesis in children via transcriptional profiling of the airway epithelium', JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, 145 1562-1573 (2020) [C1]
DOI 10.1016/j.jaci.2020.02.018
Citations Scopus - 1Web of Science - 1
Co-authors Darryl Knight, Andrew Reid, Peter Wark
2020 Reid AT, Nichol KS, Veerati PC, Moheimani F, Kicic A, Stick SM, et al., 'Blocking notch3 signaling abolishes MUC5AC production in airway epithelial cells from individuals with asthma', American Journal of Respiratory Cell and Molecular Biology, 62 513-523 (2020) [C1]

Copyright © 2020 by the American Thoracic Society. In asthma, goblet cell numbers are increased within the airway epithelium, perpetuating the production of mucus that is more dif... [more]

Copyright © 2020 by the American Thoracic Society. In asthma, goblet cell numbers are increased within the airway epithelium, perpetuating the production of mucus that is more difficult to clear and results in airway mucus plugging. Notch1, Notch2, or Notch3, or a combination of these has been shown to influence the differentiation of airway epithelial cells. How the expression of specific Notch isoforms differs in fully differentiated adult asthmatic epithelium and whether Notch influences mucin production after differentiation is currently unknown. We aimed to quantify different Notch isoforms in the airway epithelium of individuals with severe asthma and to examine the impact of Notch signaling on mucin MUC5AC. Human lung sections and primary bronchial epithelial cells from individuals with and without asthma were used in this study. Primary bronchial epithelial cells were differentiated at the air-liquid interface for 28 days. Notch isoform expression was analyzed by Taqman quantitative PCR. Immunohistochemistry was used to localize and quantify Notch isoforms in human airway sections. Notch signaling was inhibited in vitro using dibenzazepine or Notch3-specific siRNA, followed by analysis of MUC5AC. NOTCH3 was highly expressed in asthmatic airway epithelium compared with nonasthmatic epithelium. Dibenzazepine significantly reduced MUC5AC production in air-liquid interface cultures of primary bronchial epithelial cells concomitantly with suppression of NOTCH3 intracellular domain protein. Specific knockdown using NOTCH3 siRNA recapitulated the dibenzazepine-induced reduction in MUC5AC. We demonstrate that NOTCH3 is a regulator of MUC5AC production. Increased NOTCH3 signaling in the asthmatic airway epithelium may therefore be an underlying driver of excess MUC5AC production.

DOI 10.1165/rcmb.2019-0069OC
Citations Scopus - 3Web of Science - 3
Co-authors Darryl Knight, Philip Hansbro, Christopher Grainge, Peter Wark, Nathan Bartlett, Fatemeh Moheimani, Andrew Reid
2020 Tasoulis T, Silva A, Veerati PC, Baker M, Hodgson WC, Dunstan N, Isbister GK, 'Intra-Specific Venom Variation in the Australian Coastal Taipan Oxyuranus scutellatus', Toxins, 12 (2020) [C1]
DOI 10.3390/toxins12080485
Co-authors Mark Baker, Geoffrey Isbister
2020 Veerati PC, Troy NM, Reid AT, Li NF, Nichol KS, Kaur P, et al., 'Airway Epithelial Cell Immunity Is Delayed During Rhinovirus Infection in Asthma and COPD', Frontiers in Immunology, 11 (2020)

© Copyright © 2020 Veerati, Troy, Reid, Li, Nichol, Kaur, Maltby, Wark, Knight, Bosco, Grainge and Bartlett. Respiratory viral infections, particularly those caused by rhinovirus,... [more]

© Copyright © 2020 Veerati, Troy, Reid, Li, Nichol, Kaur, Maltby, Wark, Knight, Bosco, Grainge and Bartlett. Respiratory viral infections, particularly those caused by rhinovirus, exacerbate chronic respiratory inflammatory diseases, such as asthma and chronic obstructive pulmonary disease (COPD). Airway epithelial cells are the primary site of rhinovirus replication and responsible of initiating the host immune response to infection. Numerous studies have reported that the anti-viral innate immune response (including type I and type III interferon) in asthma is less effective or deficient leading to the conclusion that epithelial innate immunity is a key determinant of disease severity during a rhinovirus induced exacerbation. However, deficient rhinovirus-induced epithelial interferon production in asthma has not always been observed. We hypothesized that disparate in vitro airway epithelial infection models using high multiplicity of infection (MOI) and lacking genome-wide, time course analyses have obscured the role of epithelial innate anti-viral immunity in asthma and COPD. To address this, we developed a low MOI rhinovirus model of differentiated primary epithelial cells obtained from healthy, asthma and COPD donors. Using genome-wide gene expression following infection, we demonstrated that gene expression patterns are similar across patient groups, but that the kinetics of induction are delayed in cells obtained from asthma and COPD donors. Rhinovirus-induced innate immune responses were defined by interferons (type-I, II, and III), interferon response factors (IRF1, IRF3, and IRF7), TLR signaling and NF-¿B and STAT1 activation. Induced gene expression was evident at 24 h and peaked at 48 h post-infection in cells from healthy subjects. In contrast, in cells from donors with asthma or COPD induction was maximal at or beyond 72¿96 h post-infection. Thus, we propose that propensity for viral exacerbations of asthma and COPD relate to delayed (rather than deficient) expression of epithelial cell innate anti-viral immune genes which in turns leads to a delayed and ultimately more inflammatory host immune response.

DOI 10.3389/fimmu.2020.00974
Co-authors Peter Wark, Darryl Knight, Steven Maltby, Andrew Reid, Christopher Grainge, Nathan Bartlett
2020 Veerati PC, Mitchel JA, Reid AT, Knight DA, Bartlett NW, Park J-A, Grainge CL, 'Airway mechanical compression: its role in asthma pathogenesis and progression.', Eur Respir Rev, 29 (2020)
DOI 10.1183/16000617.0123-2019
Co-authors Andrew Reid, Nathan Bartlett, Christopher Grainge, Darryl Knight
2019 Veerati PC, Grainge C, 'Peering deeper into asthmatic lungs', RESPIROLOGY, 24 1037-1038 (2019)
DOI 10.1111/resp.13625
Co-authors Christopher Grainge
2019 Singanayagam A, Loo SL, Calderazzo M, Finney LJ, Torralbo MBT, Bakhsoliani E, et al., 'Antiviral immunity is impaired in COPD patients with frequent exacerbations', American Journal of Physiology - Lung Cellular and Molecular Physiology, 317 L893-L903 (2019) [C1]

© the American Physiological Society. Patients with frequent exacerbations represent a chronic obstructive pulmonary disease (COPD) subgroup requiring better treatment options. Th... [more]

© the American Physiological Society. Patients with frequent exacerbations represent a chronic obstructive pulmonary disease (COPD) subgroup requiring better treatment options. The aim of this study was to determine the innate immune mechanisms that underlie susceptibility to frequent exacerbations in COPD. We measured sputum expression of immune mediators and bacterial loads in samples from patients with COPD at stable state and during virusassociated exacerbations. In vitro immune responses to rhinovirus infection in differentiated primary bronchial epithelial cells (BECs) sampled from patients with COPD were additionally evaluated. Patients were stratified as frequent exacerbators (=2 exacerbations in the preceding year) or infrequent exacerbators (<2 exacerbations in the preceding year) with comparisons made between these groups. Frequent exacerbators had reduced sputum cell mRNA expression of the antiviral immune mediators type I and III interferons and reduced interferon-stimulated gene (ISG) expression when clinically stable and during virus-associated exacerbation. A role for epithelial cellintrinsic innate immune dysregulation was identified: induction of interferons and ISGs during in vitro rhinovirus (RV) infection was also impaired in differentiated BECs from frequent exacerbators. Frequent exacerbators additionally had increased sputum bacterial loads at 2 wk following virus-associated exacerbation onset. These data implicate deficient airway innate immunity involving epithelial cells in the increased propensity to exacerbations observed in some patients with COPD. Therapeutic approaches to boost innate antimicrobial immunity in the lung could be a viable strategy for prevention and treatment of frequent exacerbations.

DOI 10.1152/ajplung.00253.2019
Citations Scopus - 8Web of Science - 8
Co-authors Peter Wark, Nathan Bartlett, Andrew Reid, Jason Girkin, Christopher Grainge
2018 Reid AT, Veerati PC, Gosens R, Bartlett NW, Wark PA, Grainge CL, et al., 'Persistent induction of goblet cell differentiation in the airways: Therapeutic approaches', Pharmacology and Therapeutics, 185 155-169 (2018) [C1]

© 2017 Dysregulated induction of goblet cell differentiation results in excessive production and retention of mucus and is a common feature of several chronic airways diseases. To... [more]

© 2017 Dysregulated induction of goblet cell differentiation results in excessive production and retention of mucus and is a common feature of several chronic airways diseases. To date, therapeutic strategies to reduce mucus accumulation have focused primarily on altering the properties of the mucus itself, or have aimed to limit the production of mucus-stimulating cytokines. Here we review the current knowledge of key molecular pathways that are dysregulated during persistent goblet cell differentiation and highlights both pre-existing and novel therapeutic strategies to combat this pathology.

DOI 10.1016/j.pharmthera.2017.12.009
Citations Scopus - 12Web of Science - 11
Co-authors Christopher Grainge, Andrew Reid, Fatemeh Moheimani, Nathan Bartlett, Peter Wark, Philip Hansbro, Darryl Knight
2018 Singanayagam A, Glanville N, Girkin JL, Ching YM, Marcellini A, Porter JD, et al., 'Corticosteroid suppression of antiviral immunity increases bacterial loads and mucus production in COPD exacerbations', NATURE COMMUNICATIONS, 9 (2018) [C1]
DOI 10.1038/s41467-018-04574-1
Citations Scopus - 37Web of Science - 35
Co-authors Jason Girkin, Andrew Reid, Darryl Knight, Christopher Grainge, Peter Wark, Nathan Bartlett
Show 7 more journal articles

Conference (3 outputs)

Year Citation Altmetrics Link
2018 Veerati P, Reid A, Nichol K, Ngan L, Teresa W, Wark PAB, et al., 'A Physiological Relevant Rhinovirus Infection Model in Differentiated Human Primary Bronchial Epithelial Cells from Healthy, Asthmatic and COPD Donors', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, San Diego, CA (2018)
Co-authors Darryl Knight, Christopher Grainge, Nathan Bartlett, Peter Wark
2018 Veerati P, Bartlett NW, Nichol K, Wark PAB, Knight DA, Grainge CL, 'Mechanical Forces Suppress Innate Anti-Viral Immunity in Primary Human Airway Epithelial Cells Obtained from Asthma Donors', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, San Diego, CA (2018)
Co-authors Peter Wark, Nathan Bartlett, Darryl Knight, Christopher Grainge
2017 Veerati P, Bartlett N, Parsons K, Moheimani F, Wark P, Knight D, Grainge C, 'MECHANICAL FORCES ATTENUATE ANTI-VIRAL IMMUNITY IN PRIMARY HUMAN AIRWAY EPITHELIAL CELLS FROM ASTHMATIC DONORS', RESPIROLOGY (2017)
Co-authors Peter Wark, Fatemeh Moheimani, Nathan Bartlett, Christopher Grainge, Darryl Knight
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Grants and Funding

Summary

Number of grants 6
Total funding $89,782

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


20201 grants / $10,000

Is asthma medication protective against coronavirus infection?$10,000

Asthmatics who are more susceptible to most viral infections appear to be under-represented with COVID-19. Asthma medications such as β-agonists, steroids and combination therapies might have a serendipitous effect against CoV2 infection by suppressing airway ACE2 expression and thereby reducing the viral entry into the host primary airway epithelial cells. 

Funding body: School of Medicine and Public Health, Faculty of Health and Medicine, University of Newcastle

Funding body School of Medicine and Public Health, Faculty of Health and Medicine, University of Newcastle
Project Team

Dr. Punnam Chander Veerati, Dr. Su-Ling Loo, Mrs. Kristy Nichol, Dr. Andrew Reid, Dr. Alan Hsu, Dr. Peter Wark, Dr. Nathan Bartlett, Dr. Christopher Grainge

Scheme 2020 UoN SMPH Strategic Pilot Grant
Role Lead
Funding Start 2020
Funding Finish 2020
GNo
Type Of Funding Internal
Category INTE
UON N

20193 grants / $38,725

The role of apical mechanical shear stress on epithelial cell function in asthma$32,225

Funding body: John Hunter Hospital Charitable Trust

Funding body John Hunter Hospital Charitable Trust
Project Team Doctor Andrew Reid, Doctor Punnam Chander Veerati, Conjoint Associate Professor Christopher Grainge, Conjoint Associate Professor Christopher Grainge
Scheme Research Grant
Role Investigator
Funding Start 2019
Funding Finish 2020
GNo G1900261
Type Of Funding C2220 - Aust StateTerritoryLocal - Other
Category 2220
UON Y

2019 FHEAM Equipment Grant$3,500

This grant was awarded to purchase a set of single-channel laboratory pipettes and a manual 8-channel and digital 12-channel pipettes for virus lab.

Funding body: Faculty of Health and Medicine, The University of Newcastle

Funding body Faculty of Health and Medicine, The University of Newcastle
Project Team

Doctor Punnam Veerati, Doctor Andrew Reid, Doctor Su-Ling Loo, Associate Professor Nathan Bartlett, Conjoint Associate Professor Christopher Grainge

Scheme Equipment grant
Role Lead
Funding Start 2019
Funding Finish 2019
GNo
Type Of Funding Internal
Category INTE
UON N

2019 PRC travel grant$3,000

Funding body: Priority Research Centre for Healthy Lungs

Funding body Priority Research Centre for Healthy Lungs
Scheme Priority Research Centre for Healthy Lungs
Role Lead
Funding Start 2019
Funding Finish 2019
GNo
Type Of Funding Internal
Category INTE
UON N

20182 grants / $41,057

Establishing a comprehensive in vitro model of bronchiectasis$23,750

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Conjoint Associate Professor Christopher Grainge, Doctor Andrew Reid, Conjoint Professor Peter Wark, Doctor Katie Baines, Doctor Benjamin Vaughan, Doctor Punnam Chander Veerati
Scheme Research Grant
Role Investigator
Funding Start 2018
Funding Finish 2020
GNo G1901576
Type Of Funding C3120 - Aust Philanthropy
Category 3120
UON Y

The role of apical mechanical shear stress on epithelial cell function in asthma$17,307

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Doctor Andrew Reid, Doctor Punnam Chander Veerati, Conjoint Associate Professor Christopher Grainge
Scheme Project Grant
Role Investigator
Funding Start 2018
Funding Finish 2018
GNo G1800434
Type Of Funding C3112 - Aust Not for profit
Category 3112
UON Y
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Dr Punnam Chander Veerati

Position

Postdoctoral Researcher
School of Medicine and Public Health
Faculty of Health and Medicine

Contact Details

Email punnam.veerati@newcastle.edu.au
Phone (02) 40420610

Office

Room Rm 2109, Level 2 West, HMRI
Building Hunter Medical Research Institute (HMRI)
Location HMRI

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