AM J PHYSIOL-GASTR L:肠道SOCS3蛋白调控炎症性肠病发展
来源:生物谷 2015-03-06 11:00
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。&n
2015年3月6日 讯 /生物谷BIOON/ --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。
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.
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