Molecular mechanism of T-cell control of Chlamydia in mice: Role of nitric oxide in vivo
Molecular mechanism of T-cell control of Chlamydia in mice: Role of nitric oxide in vivo
复制标题
DOI：
10.1046/j.1365-2567.1996.d01-655.x
复制
发表时间：
1996-05-01
期刊：
影响因子：
6.4
通讯作者：
Igietseme, JU
中科院分区：
文献类型：
--
作者：
Igietseme, JU
T细胞介导的免疫对于控制小鼠中的衣原体至关重要。最近的证据表明，在体外模型的粘膜上皮细胞，极化上皮细胞淋巴细胞共培养（PELC）系统的研究表明，保护鼠T细胞介导的沙眼衣原体剂的小鼠肺炎（MoPn）的细胞内抑制至少部分激活干扰素-γ（IFN-γ）诱导型一氧化氮合酶（iNOS）途径。为了研究一氧化氮是否在体内控制衣原体感染中发挥作用，在存在特异性iNOS抑制剂的情况下，在小鼠中分析了衣原体特异性T细胞克隆（克隆2.14-0）的保护能力。结果表明，该克隆在体内清除衣原体的能力部分是通过诱导一氧化氮（NO）的产生介导的。L-精氨酸类似物和iNOS抑制剂N-G-单甲基-L-精氨酸单乙酸酯（MLA）增加了感染小鼠中的衣原体负荷，并抑制了克隆2.14-0清除体内生殖器MoPn感染的能力。结果与IFN-γ诱导型iNOS途径参与小鼠T淋巴细胞对衣原体的控制的工作假设一致。
T-cell-mediated immunity is crucial for the control of Chlamydia in mice. Recent evidence from studies in an in vitro model of the mucosal epithelium, the polarized epithelial-lymphocyte coculture (PELC) system, indicated that protective murine T cells mediated intracellular inhibition of the Chlamydia trachomatis agent of mouse pneumonitis (MoPn) at least partly by activating the interferon-gamma (IFN-gamma)-inducible nitric oxide synthase (iNOS) pathway. To investigate whether nitric oxide played a role in controlling chlamydial infection in vivo, the protective capacity of a chlamydial-specific T-cell clone (clone 2.14-0) was analysed in mice in the presence of a specific inhibitor of iNOS. The results revealed that the ability of this clone to clear Chlamydia in vivo is in part mediated by induction of nitric oxide (NO) production. The L-arginine analogue and iNOS inhibitor, N-G-monomethyl-L-arginine monoacetate (MLA), increased the chlamydial burden in infected mice and inhibited the ability of clone 2.14-0 to clear genital MoPn infection in vivo. The results are consistent with the working hypothesis that the IFN-gamma-inducible iNOS pathway is involved in the control of Chlamydia by T lymphocytes in mice.