根据Lancaster大学科学家开展的一项研究发现：炎性肠病(IBD)的发展会受到肠道中一种能导致炎症的蛋白质的影响。

        在英国，每百人中有一人在其一生中将罹患IBD，包括克罗恩病和溃疡性结肠炎。肠衬里被修复的速度取决于其与肠道中细菌的相互作用。Lancaster大学的Rachael Rigby医生说：在发达国家IBD发病增加的潜在原因包括人们肠道微生物的改变。肠道微生物的改变影响肠衬里被修复的速度，肠衬里提供了抵御肠道内传染性病原体的第一道防线。整个肠道衬有单层上皮细胞，在IBD情况下，单层上皮细胞UI发炎和被毁坏。与来自Lancaster大学的Imtiyaz Thagia等合作，Rigby医生研究了肠道中名为SOCS3蛋白质的作用(在IBD情况下SOCS3会增加)。这项研究由Medical Research Council资助，发表在American Journal of Physiology杂志上。蛋白质SOCS3会限制肠道炎症，但研究人员发现，其在IBD情况下，SOCS3的增加对上皮衬里的修复会产生负面影响。Rigby医生说：我们的最新研究报告显示，SOCS3会限制微生物诱导上皮伤口愈合。这些结果提供了进一步的证据支持上皮SOCS3在肠道健康中的调节作用，提示SOCS3的表达增加在IBD炎症中发挥重要作用。

        doi:10.1152/ajpgi.00214.2014

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Intestinal epithelial suppressor of cytokine signaling 3 enhances microbial-induced inflammatory tumor necrosis factor-α, contributing to epithelial barrier dysfunction

        Rachael Rigby， et al.

        ABSTRACT A single layer of intestinal epithelial cells (IEC) lines the entire GI tract and provides the first line of defence and barrier against an abundance of microbial stimuli. IEC homeostasis and repair are mediated through microbe-sensing Toll-like receptor (TLR)-induced inflammatory pathways. Increasing evidence supports a role of suppressor of cytokine signaling 3 (SOCS3) as a modulator of IEC turnover, balancing controlled repair and replenishment with excessive IEC proliferation predisposing to dysplasia and cancer. Our data indicate that SOCS3 can limit microbial-induced epithelial repair, promote TNFα, possibly through limiting TNFR2 expression in intestinal epithelial cells (IEC). Activation of TLR5 signalling pathways, compared with other TLR, increase TNFα mRNA in a dose dependent manner and SOCS3 enhances TLR5-induced TNFα. We also show that flagellin promotes transcription of TNFR2 and that SOCS3 may limit this expression, presenting a mechanism of SOCS3 action. Our data also supports the role of microbial ligands in epithelial wound healing and suggests that a functional consequence of increased TNFα is reduced wound healing. These results provide further evidence to support the regulatory role of epithelial SOCS3 in intestinal health and suggest that the increased expression of SOCS3 observed in IBD may serve to perpetuate 'inflammation' by promoting TNFα production and limiting epithelial repair in response to commensal microflora.