TLR2/TLR4 activation induces Tregs and suppresses intestinal inflammation caused by Fusobacterium nucleatum in vivo.
TLR2/TLR4 activation induces Tregs and suppresses intestinal inflammation caused by Fusobacterium nucleatum in vivo.
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TLR2/TLR4 激活诱导 Tregs 并抑制体内具核梭杆菌引起的肠道炎症
DOI：
10.1371/journal.pone.0186179
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发表时间：
2017
期刊：
影响因子：
3.7
通讯作者：
Tang B
中科院分区：
文献类型：
--
作者：
Jia YP;Wang K;Zhang ZJ;Tong YN;Han D;Hu CY;Li Q;Xiang Y;Mao XH;Tang B
Toll样受体2和Toll样受体4在核梭杆菌感染引起的肠道炎症中起重要作用，但TLR2/TLR4在促炎细胞因子调控中的作用尚不清楚。在本研究中，通过基因芯片分析和qRT-PCR，我们发现TLR2/TLR4参与了核假单胞菌诱导的Caco-2细胞、C57BL/6小鼠和人类临床标本的炎症信号通路。在TLR2-/-和TLR4-/-小鼠中，核孢子虫感染导致细菌定植增加，并产生促炎细胞因子IL-8、IL-1β和肿瘤坏死因子-α。此外，TLR2-/-和TLR4-/-小鼠Foxp3+CD4+T细胞占总CD4+T细胞的比例低于野生型小鼠，而杂交型小鼠高于基因敲除小鼠，提示TLR2/TLR4介导了Tregs的数量。此外，还观察到TLR2-/-小鼠在Treg转移后炎性细胞因子水平降低。因此，这些数据表明TLR2/TLR4在体内通过Tregs调节核颤菌诱导的炎性细胞因子。
Toll-like receptors (TLRs) 2 and 4 play critical roles in intestinal inflammation caused by Fusobacterium nucleatum (F. nucleatum) infection, but the role of TLR2/TLR4 in regulation of proinflammatory cytokines remains unknown. In this study, through microarray analysis and qRT-PCR, we showed that TLR2/TLR4 are involved in the F. nucleatum-induced inflammatory signaling pathway in Caco-2 cells, C57BL/6 mice and human clinical specimens. In TLR2-/- and TLR4-/- mice, F. nucleatum infection resulted in increased colonization of the bacteria and production of the proinflammatory cytokines IL-8, IL-1β and TNF-α. In addition, the ratio of Foxp3+ CD4+ T cells in the total CD4+ T cells in TLR2-/- and TLR4-/- mice was less than that in wild-type mice, and the ratio in hybrid mice was more than that in knockout mice, which suggested that TLR2/TLR4 mediated the number of Tregs. Furthermore, it was observed that inflammatory cytokine levels were reduced in TLR2-/- mice after Treg transfer. Thus, these data indicate that TLR2/TLR4 regulate F. nucleatum-induced inflammatory cytokines through Tregs in vivo.
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