Oral Inflammation & Innate Immunity Group
Professor Glen Scholz
Our group’s major objective is to understand how host‒microbe homeostasis in the oral cavity is maintained. This is important because the disruption of homeostasis causes various oral inflammatory diseases (e.g. periodontitis) as well as exacerbates systemic inflammatory diseases. Thus, we want to understand the mechanisms that enable the innate immune system to maintain immunological homeostasis with commensal bacteria whilst preventing infection by pathogens. We employ a range of experimental systems in our research, including genetically-modified mice, coupled with cell culture systems. This is complemented by various technologies and experimental approaches, including gene expression profiling, cell signalling pathway analysis, mass spectrometry-based proteomics, and cell imaging.
Understanding how oral mucosal epithelial cells tailor different immune responses to commensal bacteria and pathogens
Oral mucosal epithelial cells express innate immune receptors that enable the detection of bacteria. However, how these cells tolerate commensal bacteria and yet stimulate inflammation in response to pathogens is poorly understood. Our latest research indicates the spatial context in which bacteria are detected by epithelial cells within the oral mucosa plays a critical instructive role in enabling the cells to discriminate between commensal bacteria and pathogens and thereby respond appropriately. You will build on this novel research by investigating how spatiotemporal regulation of mucosal inflammatory pathways could enable differentially-tailored immune responses to commensal bacteria and pathogens.
Deciphering an epithelial cell intrinsic TLR2‒IL 36γ axis in oral mucosal immunity and homeostasis
The oral cavity is a major entry portal for many important bacterial pathogens. Our latest research indicates the innate immune receptor TLR2 and the novel inflammatory cytokine Interleukin 36 gamma (IL 36γ) function as an epithelial cell intrinsic axis to orchestrate the host response to bacteria; for example, regulating expression of cytokines that recruit specific immune cell subsets (e.g. T helper cells). Using gene knockout mice and cell culture systems, you will build on this novel research and elucidate how the TLR2‒IL 36γ axis orchestrates oral mucosal immunity to maintain host‒microbe homeostasis.
How the IRF6 transcription factor regulates oral mucosal immunity and homeostasis
We have previously established that IRF6 directly regulates specific Toll-like receptor-mediated host defence functions of oral epithelial cells by regulating the expression of inflammatory genes. Our latest research indicates IRF6 also indirectly regulates their host defence functions via its control of epithelial cell terminal differentiation. This is important because our latest research indicates that epithelial differentiation may enable spatiotemporal control of immune responses to bacteria in the oral mucosa. You will build on this novel research by elucidating how IRF6 enables spatiotemporal regulation of oral mucosal inflammatory pathways.
Elucidating how bacterial metabolites can disrupt host-microbe homeostasis in the oral mucosa
The innate immune system is activated by structural components of bacteria (e.g. lipopeptides). However, bacterial metabolic products, such as short-chain fatty acids (SCFA), have emerged as important modulators of innate immune cell activation via both epigenetic and non-epigenetic mechanisms. We have found that SCFA also modulate specific host defence functions of oral mucosal epithelial cells. This is important because it may help to explain how dysbiosis disrupts host microbe homeostasis and promotes inflammation in the oral mucosa. You will build on this novel research by investigating the mechanisms underlying the effects of bacterial SCFA on oral mucosal epithelial cell host defence functions.
For project inquiries, contact our research group head.
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For further information about this research, please contact Head of Research Group Professor Glen Scholz
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