Dr Simon Johnston
PhD
Department of Infection, Immunity and Cardiovascular Disease
Senior Research Fellow
+44 114 222 2301
Full contact details
Department of Infection, Immunity and Cardiovascular Disease
Firth Court
Western Bank
Sheffield
S10 2TN
- Profile
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- 2018 - Senior Research Fellow. Department of Infection, Immunity and Cardiovascular Disease, Bateson Centre, University of Sheffield.
- 2012 - 2018 Medical Research Council - Career Development Award Fellow, Department of Infection, Immunity and Cardiovascular Disease, MRC Centre for Developmental and Biomedical Genetics. (2012-2014) and Bateson Centre (2014), University of Sheffield.
- 2012 - 2017 Krebs Institute - Fellow, Krebs Institute, University of Sheffield.
- 2011 - 2012 Lister Institute Post-Doctoral Research Associate, University of Birmingham, Birmingham.
- 2010 - 2011 Wellcome Trust - Post-Doctoral Research Associate, University of Birmingham, Birmingham.
- 2007 - 2010 Medical Research Council - Post-Doctoral Research Associate, University of Birmingham, Birmingham.
- 2003 - 2007 PhD Cell Biology, University of Birmingham.
- 2000 - 2003 BSc (Hons) Biochemistry, University of Birmingham.
- Research interests
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My research group is focused on the study infectious disease to improve patient treatment and to further our fundamental understanding of how the immune system functions. We use a multidisciplinary approach in collaboration with biologists, clinicians, engineers and physicists. In this way we aim to use the best experimental model to answer the specific research question at hand.
We have a particular interest in opportunistic fungal infections in immunocompromise. One example is Cryptococcus neoformans, which is a fungal pathogen of humans and causes hundreds of thousands of deaths in the severely immunocompromised world-wide each year.
Most life-threatening infections are in individuals with AIDS in Africa where it is the most common cause of meningo-encephalitis and the cause of 15% of AIDS-related deaths. In our studies of cryptococcal disease my group has contributed to how the immune system is defective in responding to cryptococcal infection in immunocompromise and what features of cryptococci drive their virulence.
Currently, we have three research priorities:
- Macrophage mediated immunity to opportunistic infection
- Central nervous system pathology in infection and immune system disease
- Mechanisms and regulation of phagocytosis
- Publications
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Journal articles
- 15-keto-prostaglandin E2 activates host peroxisome proliferator-activated receptor gamma (PPAR-γ) to promote Cryptococcus neoformans growth during infection. PLoS Pathogens, 15(3). View this article in WRRO
- Cryptococcus neoformans escape from Dictyostelium amoeba by both WASH-mediated constitutive exocytosis and vomocytosis. Frontiers in Cellular and Infection Microbiology, 8. View this article in WRRO
- A transgenic zebrafish model for the
in vivo
study of the blood and choroid plexus brain barriers using
claudin 5. Biology Open, 7(2), bio030494-bio030494. View this article in WRRO
- The cause and effect of Cryptococcus interactions with the host.. Curr Opin Microbiol, 40, 88-94. View this article in WRRO
- Vomocytosis of live pathogens from macrophages is regulated by the atypical MAP kinase ERK5. Science Advances, 3(8). View this article in WRRO
- Cryptococcus neoformans Intracellular Proliferation and Capsule Size Determines Early Macrophage Control of Infection. Scientific Reports, 6(1), 21489-21489. View this article in WRRO
- Cryptococcus neoformans Thermotolerance to Avian Body Temperature Is Sufficient For Extracellular Growth But Not Intracellular Survival In Macrophages. Scientific Reports, 6. View this article in WRRO
- Immunity to Cryptococcus neoformans and C. gattii during cryptococcosis. Fungal Genetics and Biology, 78, 76-86. View this article in WRRO
- ‘Division of labour’ in response to host oxidative burst drives a fatal Cryptococcus gattii outbreak. Nature Communications, 5, 5194-5194. View this article in WRRO
- Cryptococcus interactions with macrophages: evasion and manipulation of the phagosome by a fungal pathogen.. Cell Microbiol, 15(3), 403-411.
- The human fungal pathogen Cryptococcus neoformans escapes macrophages by a phagosome emptying mechanism that is inhibited by arp2/3 complex- mediated actin polymerisation. PLoS Pathogens, 6(8), 27-28.
- 15-keto-prostaglandin E2 activates host peroxisome proliferator-activated receptor gamma (PPAR-γ) to promote Cryptococcus neoformans growth during infection. PLoS Pathogens, 15(3). View this article in WRRO