Induction of alpha/beta interferon and dependent nitric oxide synthesis during Chlamydia trachomatis infection of McCoy cells in the absence of exogenous cytokine
Induction of alpha/beta interferon and dependent nitric oxide synthesis during Chlamydia trachomatis infection of McCoy cells in the absence of exogenous cytokine
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DOI：
10.1128/iai.64.10.3951-3956.1996
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发表时间：
1996-10-01
影响因子：
3.1
通讯作者：
Pearce, JH
中科院分区：
文献类型：
--
作者：
Devitt, A;Lund, PA;Pearce, JH
检查了两种沙眼衣原体菌株（L2/434/Bu [生物变种 LGV] 和 E/DK20/ON [生物变种沙眼]）在感染 McCoy（小鼠）细胞培养物时诱导假定宿主防御反应的倾向，两种菌株均诱导 McCoy 细胞产生 α/β 干扰素和一氧化氮 (NO)，NO 合成是由 NO 合酶的诱导型异构体，如放线菌酮或精氨酸类似物 N-G-单甲基-L-精氨酸消除 NO 产生的能力所示；反应的程度取决于所用衣原体的剂量，感染前用氯霉素孵育 McCoy 细胞会减少菌株 434 的 NO 产生，但不会减少 DK2O 的 NO 产生，这表明最初的衣原体代谢对于 LGV 菌株的诱导至关重要。抗体抑制研究表明，NO 合成依赖于 α/β 干扰素的产生和通过诱导 总的来说，我们的研究结果表明，在没有外源细胞因子的情况下，衣原体能够在小鼠成纤维细胞中诱导干扰素和NO。然而，NO作为抗衣原体效应物的作用无法得到明确证明，因为用精氨酸类似物治疗在抑制NO产生的同时，并没有一致地增加感染细胞数量。
The propensity of two Chlamydia trachomatis strains (L2/434/Bu [biovar LGV] and E/DK20/ON [biovar trachoma]) to induce putative host defense responses upon infection of McCoy (mouse) cell cultures was examined, Both strains induced production of alpha/beta interferon and nitric oxide (NO) by McCoy cells, NO synthesis was mediated by the inducible isoform of NO synthase as indicated by the ability of cycloheximide or the arginine analog N-G-monomethyl-L-arginine to abolish NO production; the extent of the response was dependent upon the dose of chlamydiae applied, Incubation of McCoy cells with chloramphenicol prior to infection reduced NO production by strain 434 but not by DK2O, suggesting that initial chlamydial metabolism was essential to induction by the LGV strain, Antibody inhibition studies indicated that NO synthesis was dependent upon production of alpha/beta interferon and induction via lipopolysaccharide, Overall, our findings show that chlamydiae are capable of the induction of interferon and NO in murine fibroblasts in the absence of exogenous cytokines, However, the role of NO as an antichlamydial effector could not be clearly demonstrated since treatment with an arginine analog, while suppressing NO production, gave no consistent enhancement of infected cell numbers.