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    近日，來自蘭卡斯特大學(xué)的研究人員通過研究表示，炎性腸?。↖BD）的發(fā)生或許會(huì)受到腸道中引發(fā)炎癥的特殊蛋白的影響，相關(guān)研究發(fā)表于國際雜志AJP: Gastrointestinal and Liver Physiology上。

    在英國高達(dá)百分之一的人群都會(huì)在其一生中患炎性腸病，包括克羅恩病和潰瘍性結(jié)腸炎，炎性腸病在英國影響著26萬人的健康。而患者機(jī)體中小腸粘膜的修復(fù)主要依賴于腸道中細(xì)菌之間的相互作用。Rachael Rigby教授表示，為何炎性腸病患者在發(fā)達(dá)國家不斷增長，這其中潛在的原因就包括患者腸道中定居的微生物的改變等原因。

    腸道中微生物群落的改變往往會(huì)影響患者腸道粘膜的修復(fù)，而腸道粘膜為個(gè)體機(jī)體抵御感染性制劑樹起了一道有力的防線；整個(gè)腸道都由單一的上皮細(xì)胞層所覆蓋，而上皮細(xì)胞會(huì)因個(gè)體患炎性腸病而發(fā)炎以至于被破壞。文章中研究者調(diào)查了一種名為SOCS3的特殊蛋白在炎性腸病發(fā)病過程中所扮演的重要角色。

    研究者Rigby說道，SOCS3蛋白可以限制個(gè)體腸道的炎性表現(xiàn)，但其在炎性腸病患者機(jī)體中水平的增加卻對(duì)機(jī)體腸道粘膜的修復(fù)會(huì)帶來負(fù)面作用；本文研究發(fā)現(xiàn)SOCS3可以限制微生物所誘導(dǎo)的腸道上皮細(xì)胞傷口的愈合。相關(guān)研究結(jié)果為進(jìn)一步揭示SOCS3在機(jī)體腸道健康中所扮演的重要角色提供了一定的線索，同時(shí)在炎性腸病患者機(jī)體中SOCS3蛋白表達(dá)的增加同樣也會(huì)引發(fā)長期的炎性表現(xiàn)。

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    Intestinal epithelial suppressor of cytokine signaling 3 enhances microbial-induced inflammatory tumor necrosis factor-α， contributing to epithelial barrier dysfunctionImtiyaz Thagia , Elisabeth J. Shaw , Emily Smith , Kathryn J. Else , Rachael J. RigbyA single layer of intestinal epithelial cells （IEC） lines the entire gastrointestinal tract and provides the first line of defense 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 IEC repair, potentially through promoting tumor necrosis factor-α （TNF-α） and limiting TNFR2 expression. Activation of TLR5 signaling pathways, compared with other TLR, increases TNF-α mRNA in a dose-dependent manner and SOCS3 enhances TLR5-induced TNF-α。 We also show that flagellin promotes transc**tion of TNFR2 and that SOCS3 limits this expression, presenting a mechanism of SOCS3 action. Our data also support the role of microbial ligands in epithelial wound healing and suggest that a functional consequence of increased TNF-α 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 TNF-α production and limiting epithelial repair in response to commensal microflora.