Hunan Provincial Key Laboratory for Special Pathogens Prevention and Control, Hunan Province Cooperative Innovation Center for Molecular Target New Drug Study, Institute of Pathogenic Biology, Hengyang Medical College, University of South China, Hengyang, China.
Department of Clinical Laboratory Medicine, The First Affiliated Hospital, Hengyang Medical College, University of South China, Hengyang, China.
Mol Microbiol. 2024 Apr;121(4):814-830. doi: 10.1111/mmi.15232. Epub 2024 Jan 31.
Mycoplasma belong to the genus Mollicutes and are notable for their small genome sizes (500-1300 kb) and limited biosynthetic capabilities. They exhibit pathogenicity by invading various cell types to survive as intracellular pathogens. Adhesion is a crucial prerequisite for successful invasion and is orchestrated by the interplay between mycoplasma surface adhesins and specific receptors on the host cell membrane. Invasion relies heavily on clathrin- and caveolae-mediated internalization, accompanied by multiple activated kinases, cytoskeletal rearrangement, and a myriad of morphological alterations, such as membrane invagination, nuclear hypertrophy and aggregation, cytoplasmic edema, and vacuolization. Once mycoplasma successfully invade host cells, they establish resilient sanctuaries in vesicles, cytoplasm, perinuclear regions, and the nucleus, wherein specific environmental conditions favor long-term survival. Although lysosomal degradation and autophagy can eliminate most invading mycoplasmas, some viable bacteria can be released into the extracellular environment via exocytosis, a crucial factor in the prolonging infection persistence. This review explores the intricate mechanisms by which mycoplasma invades host cells and perpetuates their elusive survival, with the aim of highlighting the challenge of eradicating this enigmatic bacterium.
支原体属于柔膜体纲，其基因组大小（500-1300kb）较小，生物合成能力有限，因此具有显著特征。它们通过侵入各种细胞类型作为细胞内病原体存活来表现出致病性。黏附是成功入侵的关键前提，这是由支原体表面黏附素与宿主细胞膜上特定受体之间的相互作用所协调的。入侵严重依赖网格蛋白和 caveolae 介导的内化，伴随着多种激活的激酶、细胞骨架重排以及许多形态改变，如膜内陷、核肥大和聚集、细胞质水肿和空泡化。一旦支原体成功侵入宿主细胞，它们就在囊泡、细胞质、核周区域和核内建立了坚韧的避难所，其中特定的环境条件有利于长期存活。尽管溶酶体降解和自噬可以消除大多数入侵的支原体，但一些存活的细菌可以通过胞吐作用释放到细胞外环境中，这是延长感染持续时间的关键因素。本综述探讨了支原体侵入宿主细胞并持续存在的复杂机制，旨在强调消除这种神秘细菌的挑战。
