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Interleukin (IL)-1β: friend or foe? Unravelling the pro-inflammatory action of IL-1β in the pathogenesis of inflammatory bowel disease
▸ Coccia M, Harrison OJ, Schiering C, et al. IL-1β mediates chronic intestinal inflammation by promoting the accumulation of IL-17A secreting innate lymphoid cells and CD4+ Th17 cells. J Exp Med 2012. doi: 10.1084/jem.20111453
Patients with inflammatory bowel disease (IBD) have increased levels of IL-1β in the intestinal mucosa but there is limited knowledge on the contribution of this cytokine to intestinal pathology and the potential impact on therapeutic strategies. This recent study by Coccia and colleagues used two complementary mouse models of chronic intestinal inflammation to dissect the cellular mechanisms through which IL-1β exerts its effects. They demonstrated that IL-1β was responsible for increasing recruitment of granulocytes and activating and accumulating innate lymphoid cells (ILCs) in an experimentally induced infection model (Helicobacter hepaticus). Furthermore using a T cell transfer colitis model, they identified a key role for T cell-specific IL-1 receptor (IL-1R) signalling in pathogenic CD4+ T cells in the colon. They also demonstrated that IL-1β promotes Th17 responses from CD4+ T cells and ILCs in the intestine. The data demonstrate the beneficial effect of blocking IL-1β on reducing chronic intestinal inflammation and provide plausible mechanistic insight into its pro-inflammatory action. The findings build on the knowledge that IBD patients carrying a risk variant of the ATG16L1 gene show increased IL-1β production upon NOD2 stimulation of peripheral blood monocytes. The data provide useful insights into the multiple mechanisms through which the numerous successful IL-1β blocking therapies elicit their effects and reinforce the potential of targeting IL-1β as a therapeutic strategy in IBD.
IL-1β: friend or foe? Host response to Clostridium difficile infection
▸ Hasegawa M, Kamada N, Jiao Y, et al. Protective role of commensals against clostridium difficile infection via an IL-1b–mediated positive-feedback loop. J Immunol 2012;189:3085–91.
C difficile infection remains a significant concern in patients who are hospitalised and receiving antibiotic …
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