Following colonization of host tissues, bacterial pathogens encounter new niches in which they must gain access to nutrients and cope with stresses and defence signals generated by the host. For some pathogens, the adaptation to a new 'within-host' lifestyle involves modifications of envelope components that bear molecular patterns normally recognized by the host innate immune system. These new modified patterns limit host recognition, therefore promoting immune evasion and pathogenicity. In this review, we describe how envelope components like the peptidoglycan or lipopolysaccharide can be altered within the host to impair responses triggered by pattern recognition receptors (PRR). We also discuss the few cases reported to date of chemical modifications that occur in the envelope of some intracellular bacterial pathogens when they reside inside eukaryotic cells. These envelope alterations may have evolved due to the sentinel role performed by PRRs over pathogen-specific molecular patterns. The available data indicate that only selected pathogens seem to evade recognition due to 'within-host' envelope changes, with most of them displaying such patterns also in non host environments. Given the importance of these alterations, future studies should focus in the responsible pathogen regulators, most yet unknown, that could be targeted to prevent immune evasion.

中文翻译：

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宿主内包膜重塑及其对细菌病原体识别的影响。

在宿主组织定植后，细菌病原体遇到新的生态位，它们必须在其中获得营养并应对宿主产生的压力和防御信号。对于某些病原体，适应新的“宿主内”生活方式涉及修改具有宿主先天免疫系统通常识别的分子模式的包膜成分。这些新的修改模式限制了宿主识别，因此促进了免疫逃避和致病性。在这篇综述中，我们描述了如何在宿主内改变包膜成分（如肽聚糖或脂多糖）以削弱由模式识别受体 (PRR) 触发的反应。我们还讨论了迄今为止报道的少数几种细胞内细菌病原体驻留在真核细胞内时发生在包膜中的化学修饰的案例。这些包膜改变可能是由于 PRR 对病原体特异性分子模式的哨兵作用而进化的。现有数据表明，由于“宿主内”包膜变化，只有选定的病原体似乎逃避识别，其中大多数在非宿主环境中也显示出这种模式。考虑到这些改变的重要性，未来的研究应该集中在负责任的病原体调节剂上，这些调节剂大多是未知的，可以针对防止免疫逃避。现有数据表明，由于“宿主内”包膜变化，只有选定的病原体似乎逃避识别，其中大多数在非宿主环境中也显示出这种模式。考虑到这些改变的重要性，未来的研究应该集中在负责任的病原体调节剂上，这些调节剂大多是未知的，可以针对防止免疫逃避。现有数据表明，由于“宿主内”包膜变化，只有选定的病原体似乎逃避识别，其中大多数在非宿主环境中也显示出这种模式。考虑到这些改变的重要性，未来的研究应该集中在负责任的病原体调节剂上，这些调节剂大多是未知的，可以针对防止免疫逃避。