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首页> 外文期刊>Trends in Microbiology >The cellular paradigm of chlamydial pathogenesis
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The cellular paradigm of chlamydial pathogenesis

机译：衣原体发病机理的细胞学范例

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摘要

Diseases caused by Chlamydia are based on intense and chronic inflammation elicited and maintained by reinfection or persistent infection. The traditional view in the field is that disease is mediated by antigen-dependent delayed-type hypersensitivity or autoimmunity. This immunological paradigm has served as the basis for years of chlamydial research but the mechanism or the antigen that causes pathology has yet to be unequivocally revealed. Recent research on responses elicited in Chlamydia-infected cells defines a new direction for our understanding of this microorganism-host interaction and provides the basis for a reassessment of disease mechanisms. Chlamydia-infected non-immune mammalian cells produce proinflammatory chemokines, cytokines, growth factors and other cellular modulators. This cellular response to infection supports an alternative hypothesis for chlamydial pathogenesis are elicited by infected host cells and are necessary and sufficient to account for chronic and intense inflammation and are necessary and sufficient to account for chronic and intense inflammation and the promotion of cellular proliferation, tissue remodeling and scarring, the ultimate cause of disease sequelae.
机译：由衣原体引起的疾病基于再感染或持续感染引起并维持的强烈和慢性炎症。该领域的传统观点是疾病是由抗原依赖性迟发型超敏反应或自身免疫介导的。这种免疫学范式已成为衣原体研究多年的基础，但尚未明确揭示引起病理的机制或抗原。对衣原体感染细胞引起的反应的最新研究为我们理解这种微生物与宿主的相互作用提供了新的方向，并为重新评估疾病机理提供了基础。衣原体感染的非免疫哺乳动物细胞产生促炎性趋化因子，细胞因子，生长因子和其他细胞调节剂。这种对感染的细胞反应支持了衣原体发病机制的另一种假设，即被感染的宿主细胞引发了衣原体的发病机理，对于解释慢性和强烈炎症是必要和充分的，对于解释慢性和强烈炎症以及促进细胞增殖，组织的必要和充分的重塑和疤痕形成，是疾病后遗症的最终原因。

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