Deficiency of LIGHT signaling pathway exacerbates Chlamydia psittaci respiratory tract infection in mice

Deficiency of LIGHT signaling pathway exacerbates Chlamydia psittaci respiratory tract infection in mice
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LIGHT信号通路缺陷加剧小鼠鹦鹉热衣原体呼吸道感染

DOI:
10.1016/j.micpath.2016.10.006
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发表时间:
2016-11-01
影响因子:
3.8
通讯作者:
Chen, Lili
Chen, Lili
中科院分区:
医学3区
文献类型:
--
作者:
Cai, Hengling;Chen, Shenghua;Chen, Lili

文献摘要

被引文献

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LIGHT是免疫球蛋白超家族(IG SF)的共刺激成员,可极大地影响T细胞活化。LIGHT信号通路在衣原体感染中的作用在鹦鹉热衣原体呼吸道感染后的小鼠中进行了评估。与野生型(WT)小鼠相比,LIGHT基因敲除(KO)小鼠体重明显减轻,存活率明显降低,细菌负荷增加,感染时间延长,肺组织病理改变严重。LIGHT KO小鼠肺组织中IFN-γ、TNF-α、IL-17和IL-12的mRNA水平显著低于WT小鼠。虽然两组小鼠脾脏中CD 4(+)和CD 8(+)T细胞的百分比没有明显差异,但LIGHT KO小鼠中CD 4 + CD 25(+)FoxP 3(+)Treg细胞的百分比显著升高。总之,这些结果表明,LIGHT信号通路不仅是作为宿主对衣原体感染反应的一部分的炎性细胞因子产生所必需的,而且还影响CD 4(+)CD 25(+)FoxP 3(+)Treg细胞的分化,这两者都可能是控制衣原体感染所必需的。鹦鹉热呼吸道感染。(C)2016爱思唯尔有限公司版权所有
LIGHT, a costimulatory member of the immunoglobulin superfamily (Ig SF), can greatly impact T cell activation. The role of the LIGHT signaling pathway in chlamydial infection was evaluated in mice following respiratory tract infection with Chlamydia psittaci. Compared with wild type (WT) mice, LIGHT knockout (KO) mice showed significant reduction of body weight, much lower survival rate, higher bacterial burden, prolonged infection time courses and more severe pathological changes in lung tissue. The mRNA levels of IFN-gamma, TNF-alpha, IL-17 and IL-12 in the lung tissue of LIGHT KO mice were significantly lower than those in WT mice. While there was no obvious difference in the percentages of CD4(+) and CD8(+) T cells in the spleens of the two groups of mice, there was a markedly elevated percentage of CD4+ CD25(+) FoxP3(+) Treg cells in LIGHT KO mice. Together, these results demonstrate that the LIGHT signaling pathway is not only required for inflammatory cytokine production as part of the host response to chlamydial infection, but also influences the differentiation of CD4(+) CD25(+) FoxP3(+) Treg cells, both of which may be essential for control of C. psittaci respiratory tract infection. (C) 2016 Elsevier Ltd. All rights reserved.