Influence of the tryptophan-indole-IFNγ axis on human genital Chlamydia trachomatis infection: role of vaginal co-infections.
Influence of the tryptophan-indole-IFNγ axis on human genital Chlamydia trachomatis infection: role of vaginal co-infections.
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DOI：
10.3389/fcimb.2014.00072
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发表时间：
2014
影响因子：
5.7
通讯作者：
Belland RJ
中科院分区：
文献类型：
--
作者：
Aiyar A;Quayle AJ;Buckner LR;Sherchand SP;Chang TL;Zea AH;Martin DH;Belland RJ
生殖器沙眼衣原体感染的自然史可能有很大差异；感染可以自行消退，但也可能持续数月至数年，可能会发展成严重的病理。这种广泛变异背后的宿主和细菌因素尚不完全清楚，但强调细菌逃避/适应生殖器免疫反应的能力，和/或利用当地环境条件来生存这种免疫反应。IFNγ被认为是抗宫颈沙眼衣原体感染的主要宿主保护细胞因子。IFNγ通过诱导宿主酶吲哚胺2,3-二氧合酶起作用，该酶分解色氨酸，从而剥夺了细菌的这种必需氨基酸。体外研究表明，色氨酸剥夺导致衣原体进入一种有活力但非传染性的生长模式，这种生长模式被称为持续生长形式，其特征是独特的形态和基因表达模式。提供色氨酸可以使细菌恢复正常的发育周期。眼部和生殖器沙眼衣原体血清型抵抗色氨酸剥夺的能力有显著差异。后者独特地编码一个功能性色氨酸合成酶，通过吲哚回收合成色氨酸，如果在感染微环境中有吲哚可用。体外研究已经证实吲哚能够减轻IFNγ的影响；有人认为，受干扰的阴道微生物组可能提供体内吲哚的来源。与这一假设相一致，与细菌性阴道病相关的微生物群包括编码色氨酸酶以产生吲哚的物种。在这篇综述中，我们讨论了生殖道衣原体感染的自然历史，IFNγ对衣原体的形态学和分子变化，以及与阴道合并感染相关的微环境条件，这些微环境条件可以改善IFNγ对沙眼衣原体的影响。
The natural history of genital Chlamydia trachomatis infections can vary widely; infections can spontaneously resolve but can also last from months to years, potentially progressing to cause significant pathology. The host and bacterial factors underlying this wide variation are not completely understood, but emphasize the bacterium's capacity to evade/adapt to the genital immune response, and/or exploit local environmental conditions to survive this immune response. IFNγ is considered to be a primary host protective cytokine against endocervical C. trachomatis infections. IFNγ acts by inducing the host enzyme indoleamine 2,3-dioxgenase, which catabolizes tryptophan, thereby depriving the bacterium of this essential amino acid. In vitro studies have revealed that tryptophan deprivation causes Chlamydia to enter a viable but non-infectious growth pattern that is termed a persistent growth form, characterized by a unique morphology and gene expression pattern. Provision of tryptophan can reactivate the bacterium to the normal developmental cycle. There is a significant difference in the capacity of ocular and genital C. trachomatis serovars to counter tryptophan deprivation. The latter uniquely encode a functional tryptophan synthase to synthesize tryptophan via indole salvage, should indole be available in the infection microenvironment. In vitro studies have confirmed the capacity of indole to mitigate the effects of IFNγ; it has been suggested that a perturbed vaginal microbiome may provide a source of indole in vivo. Consistent with this hypothesis, the microbiome associated with bacterial vaginosis includes species that encode a tryptophanase to produce indole. In this review, we discuss the natural history of genital chlamydial infections, morphological and molecular changes imposed by IFNγ on Chlamydia, and finally, the microenvironmental conditions associated with vaginal co-infections that can ameliorate the effects of IFNγ on C. trachomatis.
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