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Dr Sumaira Hasnain
Dr

Sumaira Hasnain

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Overview

Background

A/Prof Sumaira Hasnain graduated with her PhD in December 2010 from The University of Manchester and is an Associate Professor at Mater Research with a team of eight researchers. A/Prof Hasnain was the first globally to demonstrate that immunity can modulate protein production in secretory cells in infection and chronic diseases. Her long-term vision has been to characterise these novel immune factors and manipulate them therapeutically using pre-clinical models of immune-driven pathologies.

A/Prof Hasnain holds a patent for targeted immunotherapy in metabolic disease which has led to the formation of a spin-off company, Jetra Therapeutics and venture capitalist funding. She has a rapid upward trajectory in research, evident by extensive body of high-quality publications including in Nature Medicine, Nature Communications, Journal of Experimental Medicine, Oncogene and Gastroenterology. She has been awarded more than $9 million in competitive funding and recently gained the National Health and Medical Research Council L1 Investigator Grant. A/Prof Hasnain has won 21 awards to date, including the Commercialisation award from The University of Queensland in 2022 and the Gastroenterological Society for Australasia; Lawrie Powell Award in 2023.

Availability

Dr Sumaira Hasnain is:
Available for supervision
Media expert

Qualifications

  • Doctor of Philosophy, The University of Manchester

Research interests

  • Understanding Immune Regulation of Cellular Stress

    Using different disease models to target cellular stress and alleviate pathology

Research impacts

We have recently described for the first time that cytokines have the ability to stop or promote protein biosynthesis via the regulation of endoplasmic reticulum (ER) stress and oxidative stress. We are targetting the immune system to repair abnormal cellular protein secretion in conditions such as diabetes, which affects 1 in 20 Australians and inflammatory bowel disease, which affects 1 in 250 Australians. This research also has implications for other diseases and infections that have a high burden on the healthcare system. The ultimate aim of this research is to devise new strategies for treatments to aid recovery following infections and to alleviate chronic inflammatory disease.

Works

Search Professor Sumaira Hasnain’s works on UQ eSpace

85 works between 2010 and 2024

41 - 60 of 85 works

2017

Journal Article

Perinatal exposure to high dietary advanced glycation end products in transgenic NOD8.3 mice leads to pancreatic beta cell dysfunction

Borg, Danielle J., Yap, Felicia Y. T., Keshvari, Sahar, Simmons, David G., Gallo, Linda A., Fotheringham, Amelia K., Zhuang, Aowen, Slattery, Robyn M., Hasnain, Sumaira Z., Coughlan, Melinda T., Kantharidis, Phillip and Forbes, Josephine M. (2017). Perinatal exposure to high dietary advanced glycation end products in transgenic NOD8.3 mice leads to pancreatic beta cell dysfunction. Islets, 10 (1), 10-24. doi: 10.1080/19382014.2017.1405189

Perinatal exposure to high dietary advanced glycation end products in transgenic NOD8.3 mice leads to pancreatic beta cell dysfunction

2017

Journal Article

Goblet cells as mucosal sentinels for immunity

McGuckin, M. A. and Hasnain, S. Z. (2017). Goblet cells as mucosal sentinels for immunity. Mucosal Immunology, 10 (5), 1118-1121. doi: 10.1038/mi.2016.132

Goblet cells as mucosal sentinels for immunity

2017

Journal Article

The effect of interleukin-22 treatment on autoimmune diabetes in the NOD mouse

Borg, Danielle J., Wang, Ran, Murray, Lydia, Tong, Hui, Steptoe, Raymond J., McGuckin, Michael A. and Hasnain, Sumaira Z. (2017). The effect of interleukin-22 treatment on autoimmune diabetes in the NOD mouse. Diabetologia, 60 (11), 1-6. doi: 10.1007/s00125-017-4392-2

The effect of interleukin-22 treatment on autoimmune diabetes in the NOD mouse

2017

Journal Article

Analyzing the properties of murine intestinal mucins by electrophoresis and histology

Wang, Ran and Hasnain, Sumaira Z. (2017). Analyzing the properties of murine intestinal mucins by electrophoresis and histology. Bio-protocol, 7 (14). doi: 10.21769/BioProtoc.2394

Analyzing the properties of murine intestinal mucins by electrophoresis and histology

2017

Journal Article

Human diseases, immunity and the oral microbiota-Insights gained from metagenomic studies

Idris, Adi, Hasnain, Sumaira Z., Huat, Lu Z. and Koh, David (2017). Human diseases, immunity and the oral microbiota-Insights gained from metagenomic studies. Oral Science International, 14 (2), 27-32. doi: 10.1016/S1348-8643(16)30024-6

Human diseases, immunity and the oral microbiota-Insights gained from metagenomic studies

2017

Conference Publication

Acute graft-versus-host disease is regulated by an IL-17-sensitive microbiome

Varelias, Antiopi, Ormerod, Kate L., Bunting, Mark D., Koyama, Motoko, Gartlan, Kate H., Kuns, Rachel D., Lachner, Nancy, Locke, Kelly R., Lim, Chun Y., Henden, Andrea S., Zhang, Ping, Clouston, Andrew D., Hasnain, Sumaira Z., McGuckin, Michael A., Blazar, Bruce R., MacDonald, Kelli P.A., Hugenholtz, Philip and Hill, Geoff R. (2017). Acute graft-versus-host disease is regulated by an IL-17-sensitive microbiome. Immunology 2017™ Meeting, Washington, DC United States, 12-16 May 2017. Rockville, MD United States: American Association of Immunologists. doi: 10.4049/jimmunol.198.supp.82.8

Acute graft-versus-host disease is regulated by an IL-17-sensitive microbiome

2017

Journal Article

Immune-driven alterations in mucin sulphation is an important mediator of Trichuris muris helminth expulsion

Hasnain, Sumaira Z., Dawson, Paul A., Lourie, Rohan, Hutson, Peter, Tong, Hui, Grencis, Richard K., McGuckin, Michael A. and Thornton, David J. (2017). Immune-driven alterations in mucin sulphation is an important mediator of Trichuris muris helminth expulsion. PLoS Pathogens, 13 (2) e1006218, e1006218. doi: 10.1371/journal.ppat.1006218

Immune-driven alterations in mucin sulphation is an important mediator of Trichuris muris helminth expulsion

2017

Journal Article

Acute graft-versus-host disease is regulated by an IL-17-sensitive microbiome

Varelias, Antiopi, Ormerod, Kate L., Bunting, Mark D., Koyama, Motoko, Gartlan, Kate H., Kuns, Rachel D., Lachner, Nancy, Locke, Kelly R., Lim, Chun Y., Henden, Andrea S., Zhang, Ping, Clouston, Andrew D., Hasnain, Sumaira Z., McGuckin, Michael A., Blazar, Bruce R., MacDonald, Kelli P. A ., Hugenholtz, Philip and Hill, Geoffrey R. (2017). Acute graft-versus-host disease is regulated by an IL-17-sensitive microbiome. Blood, 129 (15), 2172-2185. doi: 10.1182/blood-2016-08-732628

Acute graft-versus-host disease is regulated by an IL-17-sensitive microbiome

2016

Journal Article

MUC13 protects colorectal cancer cells from death by activating the NF-κB pathway and is a potential therapeutic target

Sheng, Y. H., He, Y., Hasnain, S. Z., Wang, R., Tong, H., Clarke, D. T., Lourie, R., Oancea, I., Wong, K. Y., Lumley, J. W., Florin, T. H., Sutton, P., Hooper, J. D., McMillan, N. A. and McGuckin, M. A. (2016). MUC13 protects colorectal cancer cells from death by activating the NF-κB pathway and is a potential therapeutic target. Oncogene, 36 (5), 700-713. doi: 10.1038/onc.2016.241

MUC13 protects colorectal cancer cells from death by activating the NF-κB pathway and is a potential therapeutic target

2016

Journal Article

High fat diets induce colonic epithelial cell stress and inflammation that is reversed by IL-22

Gulhane, Max, Murray, Lydia, Lourie, Rohan, Tong, Hui, Sheng, Yong H., Wang, Ran, Kang, Alicia, Schreiber, Veronika, Wong, Kuan Yau, Magor, Graham, Denman, Stuart, Begun, Jakob, Florin, Timothy H., Perkins, Andrew, Cuiv, Paraic O., McGuckin, Michael A. and Hasnain, Sumaira Z. (2016). High fat diets induce colonic epithelial cell stress and inflammation that is reversed by IL-22. Scientific Reports, 6 (1) 28990, 28990. doi: 10.1038/srep28990

High fat diets induce colonic epithelial cell stress and inflammation that is reversed by IL-22

2016

Journal Article

Oxidative and endoplasmic reticulum stress in beta-cell dysfunction in diabetes

Hasnain, Sumaira Z., Prins, Johannes B. and McGuckin, Michael A. (2016). Oxidative and endoplasmic reticulum stress in beta-cell dysfunction in diabetes. Journal of Molecular Endocrinology, 56 (2), R33-R54. doi: 10.1530/jme-15-0232

Oxidative and endoplasmic reticulum stress in beta-cell dysfunction in diabetes

2016

Conference Publication

Immune-driven alterations in mucin glycosylation are essential for Trichuris muris worm expulsion

Hasnain, S. Z., Lourie, R., Hutson, P. G., Dawson, P., Grencis, R. K. and Thornton, D. J. (2016). Immune-driven alterations in mucin glycosylation are essential for Trichuris muris worm expulsion. ICI 2016 International Congress of Immunology, Melbourne, VIC, Australia, 21-26 August 2016. Weinheim, Germany: Wiley - V C H Verlag GmbH & Co. KGaA. doi: 10.1002/eji.201670200

Immune-driven alterations in mucin glycosylation are essential for Trichuris muris worm expulsion

2016

Conference Publication

MUC13 protects colorectal cancer cells from death by activating the NF-Kb pathway and is a potential therapeutic target

Sheng, Yong H., He, Yaowu, Hasnain, Sumaira Z., Wang, Ran, Tong, Hui, Clarke, Daniel T., Lourie, Rohan, Oancea, Lulia, Wong, Kuanyau, Lumley, John W., Florin, Timothy H., Sutton, Philip, Hooper, John. D., Mcmillan, Nigel A. and Mcguckin, Michael A. (2016). MUC13 protects colorectal cancer cells from death by activating the NF-Kb pathway and is a potential therapeutic target. AACR 107th Annual Meeting on Bioinformatics and Systems Biology, New Orleans, Los Angeles, 16-20 April 2016 . Philadelphia, PA, United States: American Association for Cancer Research. doi: 10.1158/1538-7445.AM2016-3564

MUC13 protects colorectal cancer cells from death by activating the NF-Kb pathway and is a potential therapeutic target

2016

Conference Publication

High fat diets induce colonic epithelial cell stress and inflammation that is reversed by IL-22

Gulhane, M., Lourie, R., Tong, H., Kang, A., Schreiber, V., Magor, G., Denman, S., Begun, J., Florin, T., Perkins, A., O Cuiv, P., Mcguckin, M. and Hasnain, S. Z. (2016). High fat diets induce colonic epithelial cell stress and inflammation that is reversed by IL-22. ICI 2016 International Congress of Immunology, Melbourne, Australia, 21–26 August 2016. Weinheim, Germany: Wiley. doi: 10.1002/eji.201670200

High fat diets induce colonic epithelial cell stress and inflammation that is reversed by IL-22

2016

Conference Publication

Unravelling a novel mechanism by which cytokines induce ER stress to halt viral protein synthesis in mucosal epithelial cells

Hasnain, S. Z., Taylor, S., Wang, R., Chen, A., Oancea, I, Das, I, Tong, H., Florin, T., Serisier, D., Coulson, B., Mcauley, J., Lourie, R., Phipps, S. and Mcguckin, M. (2016). Unravelling a novel mechanism by which cytokines induce ER stress to halt viral protein synthesis in mucosal epithelial cells. International Congress of Immunology (ICI), Melbourne, Australia, Aug 21-26, 2016. Weinheim, Germany: Wiley - V C H Verlag GmbH & Co. KGaA. doi: 10.1002/eji.201670200

Unravelling a novel mechanism by which cytokines induce ER stress to halt viral protein synthesis in mucosal epithelial cells

2015

Conference Publication

IL-22-mediated suppression of islet inflammation

McGuckin, Mike, Hasnain, Sumaira Z., Borg, Danielle J., Loudovaris, Thomas, Kay, Thomas W., Thomas, Helen E., Whitehead, Jonathon P., Forbes, Josephine M. and Prins, John B. (2015). IL-22-mediated suppression of islet inflammation. IPITA/IXA/CTS Joint Congress, Melbourne Australia, Nov 15-19, 2015. HOBOKEN: LIPPINCOTT WILLIAMS & WILKINS.

IL-22-mediated suppression of islet inflammation

2015

Journal Article

Neutralizing IL-23 is superior to blocking IL-17 in suppressing intestinal inflammation in a spontaneous murine colitis model

Wang, Ran, Hasnain, Sumaira Z., Tong, Hui, Das, Indrajit, Che-Hao Chen, Alice, Oancea, Iulia, Proctor, Martina, Florin, Timothy H., Eri, Rajaraman D. and McGuckin, Michael A. (2015). Neutralizing IL-23 is superior to blocking IL-17 in suppressing intestinal inflammation in a spontaneous murine colitis model. Inflammatory Bowel Diseases, 21 (5), 973-984. doi: 10.1097/MIB.0000000000000353

Neutralizing IL-23 is superior to blocking IL-17 in suppressing intestinal inflammation in a spontaneous murine colitis model

2015

Journal Article

Adult non-cystic fibrosis bronchiectasis is characterised by airway luminal Th17 pathway activation

Chen, Alice C.-H., Martin, Megan L., Lourie, Rohan, Rogers, Geraint B., Burr, Lucy D., Hasnain, Sumaira Z., Bowler, Simon D., McGuckin, Michael A. and Serisier, David J. (2015). Adult non-cystic fibrosis bronchiectasis is characterised by airway luminal Th17 pathway activation. PLoS ONE, 10 (3) e0119325, e0119325. doi: 10.1371/journal.pone.0119325

Adult non-cystic fibrosis bronchiectasis is characterised by airway luminal Th17 pathway activation

2015

Conference Publication

High fat diet and the colonic mucus barrier: implications for obesity and inflammatory bowel disease

Gulhane, M., Murray, L., Wang, R., Tong, H., Mcguckin, M. and Hasnain, S. (2015). High fat diet and the colonic mucus barrier: implications for obesity and inflammatory bowel disease. Gastro 2015 GESA-AGW and WGO International Congress, Gastroenterological Society of Australia Australian Gastroenterology Week 2015 | World Congress of Gastroenterology, Brisbane, Queensland, Australia, 28 September-2 October 2015. Richmond, Australia: Wiley-Blackwell Publishing Asia. doi: 10.1111/jgh.13094

High fat diet and the colonic mucus barrier: implications for obesity and inflammatory bowel disease

2014

Journal Article

Glycemic control in diabetes is restored by therapeutic manipulation of cytokines that regulate beta cell stress

Hasnain, Sumaira Z., Borg, Danielle J., Harcourt, Brooke E., Tong, Hui, Sheng, Yonghua H., Ng, Choa Ping, Das, Indrajit, Wang, Ran, Chen, Alice C.-H., Loudovaris, Thomas, Kay, Thomas W., Thomas, Helen E., Whitehead, Jonathan P., Forbes, Josephine M., Prins, Johannes B. and McGuckin, Michael A. (2014). Glycemic control in diabetes is restored by therapeutic manipulation of cytokines that regulate beta cell stress. Nature Medicine, 20 (12), 1417-1426. doi: 10.1038/nm.3705

Glycemic control in diabetes is restored by therapeutic manipulation of cytokines that regulate beta cell stress

Funding

Current funding

  • 2025 - 2029
    Unlocking the Therapeutic Potential of Interleukin-22
    NHMRC Investigator Grants
    Open grant

Past funding

  • 2022 - 2023
    Can Targeting Interleukin-24 Resolve Intestinal Fibrosis in Inflammatory Bowel Disease?
    GESA Dr Falk Pharma Research Grant
    Open grant
  • 2020 - 2021
    Jetra/IL-22 - Project 2 - Skin toxicity, PK, dose and frequency finding studies
    UniQuest Pty Ltd
    Open grant
  • 2020
    Jetra/IL-22 - Project 1 - Confirm protein activity and human tissue profiling
    UniQuest Pty Ltd
    Open grant
  • 2020 - 2022
    Liver targeted Interleukin-22 for the treatment of non-alcoholic steatohepatitis
    NHMRC IDEAS Grants
    Open grant
  • 2019 - 2020
    Interleukin-22: New Therapeutic Target Against Viral Infections in Children
    The Children's Hospital Foundation
    Open grant
  • 2018 - 2019
    IL-22-based therapy ameliorates liver steatosis
    Gastroenterological Society of Australia
    Open grant
  • 2018 - 2022
    Targeting Immunopathology in Chronic Diseases
    NHMRC Career Development Fellowship
    Open grant
  • 2016 - 2017
    Elucidation of the Mechanism of IL-22-Mediated Suppression of Beta-Cell Stress in Diabetes
    NHMRC Project Grant
    Open grant
  • 2016
    Understanding cytokine regulation of oxidative and ER stress in infectious and inflammatory disease
    UQ Early Career Researcher
    Open grant
  • 2015 - 2017
    Cytokine Modulation of Secretory Cell Function via Oxidative and Endoplasmic Reticulum Stress in Infection and Inflammation
    UQ Postdoctoral Research Fellowship
    Open grant
  • 2015 - 2019
    IL-22 as a Suppressor of Pancreatic Beta-Cell Stress and a Treatment for Diabetes
    NHMRC Project Grant
    Open grant
  • 2015
    Pancreatic targeting of IL-22 therapy for diabetes
    UQ Collaboration and Industry Engagement Fund - Seed Research Grant
    Open grant
  • 2014 - 2015
    A new approach to tackling chemotherapy-induced mucositis
    Cancer Council Queensland
    Open grant
  • 2013 - 2015
    ER Stress as a Contributing Factor in Inflammatory Disease
    NHMRC Project Grant
    Open grant

Supervision

Availability

Dr Sumaira Hasnain is:
Available for supervision

Before you email them, read our advice on how to contact a supervisor.

Available projects

  • IL-22-based Therapy in chronic inflammatory diseases

    In a recent Nature Medicine article we demonstrate that specific inflammatory cytokines potently initiate Endoplasmic Reticulum stress by inducing oxidative stress, whilst other cytokines suppress stress and facilitate ER protein folding. While this study focused on pancreatic -cells, our data show that these stress-inducing and stress-suppressing cytokines have the same effect on intestinal, respiratory epithelial cells as well as adipocytes. In several models, including in Diabetes and IBD, we have shown that either antagonising the stress-inducing cytokines or treating with the stress-suppressing cytokines alleviates pathology. This project aims to explore this further using IL-22 based therapy.

  • Targeting IL-24 during Viral Infections

    In a collaboration with A/Prof. Simon Phipps, we have shown that IL-24 is upregulated during Pneumovirus infection. IL-24 induces cellular stress to stop protein biosynthesis and therefore might have evolved to stop viral replication in cells. We are exploring this unrecognised arm of the immune system by using different infectious models.

  • Role of the cytokine IL-22 in Wound Repair

    We are interested in exploring the role the anti-oxidant cytokine IL-22 plays following infection in aiding wound repair. Experiments designed in this project will determine whether treatment with IL-22 will enhance anti-oxidant genes, suppress cellular stress and prophylactically prevent or therapeutically resolve inflammation.

  • Disrupting Immune Responses to Reverse Fibrosis

    omedical and clinical sciences

    Project description

    Intestinal fibrosis is a debilitating complication affecting a significant portion of patients with Inflammatory Bowel Disease (IBD), including Ulcerative Colitis (UC) and Crohn's Disease (CD). Chronic inflammation within the intestinal tract leads to excessive collagen production by fibroblasts, resulting in luminal narrowing, obstruction, and a significant decline in quality of life.

    Recent studies have suggested a potential role for interleukin-24 (IL-24) in the pathogenesis of IBD. IL-24 is a cytokine with both pro-inflammatory and anti-inflammatory properties, and it has been implicated in various fibrotic diseases.

    This research aims to investigate the specific role of IL-24 in driving intestinal fibrosis in IBD, with a particular focus on its ability to activate transforming growth factor-beta (TGF-beta), a key mediator of fibrosis.

    Specific Research Questions:

    1. Expression of IL-24 and TGF-beta in fibrotic intestinal tissue: Are IL-24 and TGF-beta upregulated in fibrotic regions of the intestine in IBD patients?
    2. IL-24-mediated activation of TGF-beta: Does IL-24 directly or indirectly stimulate the production and activation of TGF-beta in intestinal fibroblasts?
    3. Role of TGF-beta in IL-24-induced fibrosis: What are the downstream effects of TGF-beta activation in promoting intestinal fibrosis?
    4. Therapeutic potential of targeting IL-24 or TGF-beta: Can inhibiting IL-24 or TGF-beta pathways be a potential therapeutic strategy for preventing or treating intestinal fibrosis in IBD?

  • The Link Between Cellular Stress and Antigen Presentation

    The endoplasmic reticulum (ER) plays a crucial role in the production and presentation of MHC Class II antigens, which are essential for the immune system to recognize and eliminate foreign invaders. When proteins are misfolded or improperly assembled in the ER, it can trigger a cellular stress response known as ER stress. This stress can impact the generation and presentation of MHC Class II antigens in several ways. Our focus has been on antigen presentation by nonprofessional antigen presenting cells like epithelial cells. Project Aim: To investigate the complex relationship between protein misfolding, ER stress, and MHC Class II antigen presentation, with a focus on understanding how these factors influence the development of immune responses, particularly those involving CD4+ T cells. Expected outcomes and deliverables: This project will be undertaken at UQ (Mater Research Institute) within the Translational Research Institute (TRI) which is a collaborative building that incorporates over 1200 research scientists and students. TRI also provides an exceptional research environment with access to state-of-art facilities including flow cytometry, microscopy and a strong network of research support professionals. There is support for PhD students, through UQ as well as Mater Student Committee (sMater). The honours student will learn a range of techniques, in particular, flow cytometry, histology, Confocal Microscopy and preclinical animal work. There is a potential of extending the honours project into a PhD project.

  • Decoding the IL-22RA1-Insulin Biosynthesis Link: A New Target for Diabetes

    The IL-22RA1 receptor is abundant in the pancreas, and external IL-22 has been shown to improve pancreatic islet health and insulin secretion. However, the natural function of IL-22RA1 signalling within these cells is incompletely understood. Our recent work has shown that endogenous IL-22RA1 signalling in regulating insulin secretion, islet regeneration, and overall metabolic health. Understanding the specific mechanisms involved in IL-22RA1-mediated regulation of pancreatic beta cell function could lead to novel therapeutic strategies for diabetes and other metabolic disorders. This project will focus on investigating the exact mechanisms by which IL-22 regulates these processes, with a particular focus on calcium storage and cytoskeletal changes. Expected outcomes and deliverables: This project will be undertaken at UQ (Mater Research Institute) within the Translational Research Institute (TRI) which is a collaborative building that incorporates over 1200 research scientists and students. TRI also provides an exceptional research environment with access to state-of-art facilities including flow cytometry, microscopy and a strong network of research support professionals. There is support for PhD students, through UQ as well as Mater Student Committee (sMater). The honours student will learn a range of techniques, in particular, flow cytometry, histology, Confocal Microscopy and preclinical animal work. There is a potential of extending the honours project into a PhD project.

Supervision history

Current supervision

Completed supervision

Media

Enquiries

Contact Dr Sumaira Hasnain directly for media enquiries about:

  • Cellular Stress
  • Immune System
  • Infectious Diseases

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