Institut Pasteur, Unité « Dynamique des interactions hôte-pathogène » and CNRS UMR3691, Université de Paris Cité, Paris, France.
Host-Pathogen Interactions in Tuberculosis Laboratory, The Francis Crick Institute, London, United Kingdom.
Front Cell Infect Microbiol. 2022 Aug 18;12:989451. doi: 10.3389/fcimb.2022.989451. eCollection 2022.
is capable of invading different host cell types including epithelial cells and M cells during local infection, and immune cells and fibroblasts during the subsequent systemic spread. The intracellular lifestyles of inside different cell types are remarkable for their distinct residential niches, and their varying replication rates. To study this, researchers have employed different cell models, such as various epithelial cells, immune cells, and fibroblasts. In epithelial cells, Typhimurium dwells within modified endolysosomes or gains access to the host cytoplasm. In the cytoplasm, the pathogen is exposed to the host autophagy machinery or poised for rapid multiplication, whereas it grows at a slower rate or remains dormant within the endomembrane-bound compartments. The swift bimodal lifestyle is not observed in fibroblasts and immune cells, and it emerges that these cells handle intracellular Typhimurium through different clearance machineries. Moreover, in these cell types . Typhimurium grows withing modified phagosomes of distinct functional composition by adopting targeted molecular countermeasures. The preference for one or the other intracellular niche and the diverse cell type-specific lifestyles are determined by the complex interactions between a myriad of bacterial effectors and host factors. It is important to understand how this communication is differentially regulated dependent on the host cell type and on the distinct intracellular growth rate. To support the efforts in deciphering invasion across the different infection models, we provide a systematic comparison of the findings yielded from cell culture models. We also outline the future directions towards a better understanding of these differential intracellular lifestyles.
能够在局部感染期间入侵不同的宿主细胞类型,包括上皮细胞和 M 细胞,以及在随后的全身传播期间入侵免疫细胞和成纤维细胞。在不同细胞类型中, 的细胞内生活方式以其独特的居住小生境和不同的复制速率为特征。为了研究这一点,研究人员采用了不同的细胞模型,如各种上皮细胞、免疫细胞和成纤维细胞。在上皮细胞中, 鼠伤寒沙门氏菌栖息在修饰的内溶酶体中或进入宿主细胞质。在细胞质中,病原体暴露于宿主自噬机制或准备快速繁殖,而在膜结合的内体室中生长速度较慢或处于休眠状态。这种快速的双模态生活方式在成纤维细胞和免疫细胞中观察不到,并且表明这些细胞通过不同的清除机制来处理细胞内的 鼠伤寒沙门氏菌。此外,在这些细胞类型中, 鼠伤寒沙门氏菌通过采用靶向分子对策,在具有不同功能组成的修饰吞噬体中生长。对一个或另一个细胞内小生境的偏好以及多样化的细胞类型特异性生活方式是由无数细菌效应因子和宿主因子之间的复杂相互作用决定的。了解这种通讯如何根据宿主细胞类型和不同的细胞内生长速率而不同地调节是很重要的。为了支持在不同感染模型中解析入侵的努力,我们对细胞培养模型产生的发现进行了系统比较。我们还概述了朝着更好地理解这些差异 细胞内生活方式的未来方向。