CD73 is critical for the resolution of murine colonic inflammation.
CD73 is critical for the resolution of murine colonic inflammation.
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DOI：
10.1155/2012/260983
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发表时间：
2012
影响因子：
--
通讯作者：
Czopik A
中科院分区：
文献类型：
--
作者：
Bynoe MS;Waickman AT;Mahamed DA;Mueller C;Mills JH;Czopik A
CD 73是糖基-磷脂酰肌醇-（GPI-）连接的膜蛋白，其催化细胞外单磷酸腺苷（AMP）去磷酸化为腺苷。腺苷是炎症的负调节剂，并防止过度的细胞损伤。我们研究了缺乏CD 73（CD 73 −/−）且不能合成胞外腺苷的小鼠在葡聚糖硫酸钠（DSS-）盐诱导的结肠炎发生过程中肠粘膜胞外腺苷的作用。我们发现，与野生型（WT）小鼠相比，CD 73 −/−小鼠对DSS诱导的结肠炎高度易感。CD 73 −/−小鼠表现出明显的体重减轻，体重恢复较慢，肠道通透性增加，紧密连接粘附分子表达减少，以及DSS去除后未解决的炎症。此外，CD 73 −/−小鼠的结肠上皮细胞表现出TLR 9表达增加、IL-1β和TNF-α水平升高以及NF-κB的组成性激活。我们的结论是，CD 73在结肠中的表达是至关重要的调节结肠免疫反应的幅度和分辨率。
CD73 is a glycosyl-phosphatidylinositol-(GPI-) linked membrane protein that catalyzes the extracellular dephosphorylation of adenosine monophosphate (AMP) to adenosine. Adenosine is a negative regulator of inflammation and prevents excessive cellular damage. We investigated the role of extracellular adenosine in the intestinal mucosa during the development of Dextran-Sulfate-Sodium-(DSS-)salt-induced colitis in mice that lack CD73 (CD73−/−) and are unable to synthesize extracellular adenosine. We have found that, compared to wild-type (WT) mice, CD73−/− mice are highly susceptible to DSS-induced colitis. CD73−/− mice exhibit pronounced weight loss, slower weight recovery, an increase in gut permeability, a decrease in expression of tight junctional adhesion molecules, as well as unresolved inflammation following the removal of DSS. Moreover, colonic epithelia in CD73−/− mice exhibited increased TLR9 expression, high levels of IL-1β and TNF-α, and constitutive activation of NF-κB. We conclude that CD73 expression in the colon is critical for regulating the magnitude and the resolution of colonic immune responses.
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