[18, 33] It is noteworthy that changes in the severity of colitis caused by IL-33 injection or

ST2 deficiency were not significantly associated with a change in body weight in the mice (Fig. S2A,B). This is consistent with a previous study showing identical Cyclopamine mw body weight loss in WT C57BL/6 and IL-33−/− mice when fed with DSS.[24] Intriguingly, compared with WT mice, the IL-33−/− mice had a delayed recovery in body weight after withdrawal of DSS.[24] However, this was not the case in ST2−/− mice in the present study and the reason is currently unclear. It may be because of the differences in genetic background of the mice and experimental conditions or the ST2-independent bioactivity of full-length IL-33 as previously suggested.[34] Furthermore, recent evidence suggests that injection of IL-33 may have a beneficial effect on chronic DSS-induced colitis or trinitrobenzene sulphonic acid-induced colitis, a model of Crohn’s disease in mice,[35, 36] suggesting that IL-33 may play a complex role in different types and throughout the duration of colitis. More studies are needed to clarify this issue. Interleukin-33 is clearly expressed in the inflamed mucosa of patients with inflammatory bowel disease, particularly in UC, and is reduced after anti-TNF-α therapy.[20-23] In these cases mucosal expression of IL-33 is also mostly localized to intestinal epithelial Pritelivir cost cells[20, 21, 23]

and in activated sub-epithelial myofibroblasts.[22] However, the clinical relevance of the IL-33/ST2 system in inflammatory bowel disease is unknown. Our results have extended these clinical findings with a putative mechanism and suggest that colon-derived IL-33 may represent an important factor for the development and exacerbation of UC. This study received financial support from the Arthritis Research UK, Medical Research Council UK and the Wellcome Trust, UK. The authors have no financial conflicts C59 chemical structure of interest. “
“Trypanosoma congolense strains have been shown to differ in their

virulence both between subgroups and within the Savannah subgroup between strains. This review revisits these findings and complements them with information on the virulence of T. congolense Savannah subgroup strains isolated from cattle (domestic transmission cycle) in different geographical areas and of strains isolated in protected areas where trypanotolerant wildlife species are the reservoir of the trypanosomes (sylvatic transmission cycle). The virulence of a total of 62 T. congolense Savannah subgroup strains (50 domestic and 12 sylvatic), determined using a standard protocol in mice, was compared. Virulence varied substantially between strains with, depending on the strain, the median survival time of infected mice varying from five to more than sixty days. The proportion of highly virulent strains (median survival time <10 days) was significantly (P = 0·005) higher in strains from the sylvatic transmission cycle.