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The regulation and consequences of immune responses during Salmonella infections

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Infections can have devastating consequences on human health. Salmonella infections provide a model to understand the impact of infection on host homeostasis and immune function as they can cause a spectrum of disease, from a self-limiting gastroenteritis to enteric fevers that are often fatal. The key factor that predicts severity is the spread of the pathogen beyond the gut, which emphasises the importance of the ability to restrict this, through the generation of granuloma-like inflammatory foci. Early control of Salmonella infection is wholly dependent upon the innate system, but clearance requires efficient Th1 responses. How these combine to effect immune control is only partially understood, as is what “success” and “failure” look like. In this talk, I will introduce two recent areas of study in the group. The first examines how the inflammatory response to Salmonella has unanticipated consequences, such as the “normal” induction of thrombosis in the vessels of infected organs, and secondly how immune cells and factors combine to help organise immunity to control infection. The key factors that I will discuss are how the timing and magnitude of immune molecules (e.g. IFNg) and cells (e.g. monocytic cells and Th1 cells) relate to bacterial localisation and the influence of this on enabling control.

This talk is part of the Babraham Seminar series.

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