Dr Sumaira Hasnain

Honorary Senior Fellow

Mater Research Institute-UQ
Faculty of Medicine

Overview

Dr Sumaira Hasnain is Senior Research Fellow and Career Track Fellow at the Mater Research Institute - University of Queensland, Brisbane, Australia. Her novel discoveries have therapeutic relevance for the treatment of multiple common inflammatory diseases including Inflammatory Bowel Disease and Diabetes.

Sumaira Hasnain’s research career started in 2006 with her PhD in infection/immunology and glycobiology, which was pivotal in defining the function of the secretory-cell barrier in infection for which she received the Distinguished Achievement Award Medal for the top postgraduate at the University of Manchester, UK. She made an important observation that secretory-cells collapsed in particular immune environment resembling Endoplasmic Reticulum stress. This was similar to work reported by Professor Michael McGuckin’s group at Mater, which prompted her move to Brisbane in 2011. This work has improved the understanding of a balanced immune response and provided new potential approaches for the treatment of a substantial number of important inflammatory and infectious diseases.

Dr Hasnain is chief investigator on three NHMRC, Cancer Council Queensland grant, UQ Collaboration and Industry Engagement Fund (CIEF) Seed Research Grant, UQ ECR grant and recently gained the UQ postdoctoral fellowship. She has published her work in top-tier journals, including a recent landmark study published in Nature medicine. Since 2010, she has won 12 awards including a Medal for Excellence in Biomedical Research from Mater Research (2012) and the prestigious 2013 QLD Premier’s Postdoctoral Research Award.

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.

Qualifications

  • Doctor of Philosophy, The University of Manchester

Publications

View all Publications

Supervision

  • Doctor Philosophy

  • Doctor Philosophy

  • Doctor Philosophy

View all Supervision

Available Projects

  • 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.

  • 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.

  • 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.

View all Available Projects

Publications

Book Chapter

Journal Article

Conference Publication

PhD and MPhil Supervision

Current Supervision

Completed Supervision

Possible Research Projects

Note for students: The possible research projects listed on this page may not be comprehensive or up to date. Always feel free to contact the staff for more information, and also with your own research ideas.

  • 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.

  • 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.

  • 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.