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.

中文翻译：

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支原体入侵宿主细胞：感染策略的综合模型

支原体属于软体动物属，以其较小的基因组大小（500-1300 kb）和有限的生物合成能力而闻名。它们通过侵入各种细胞类型并作为细胞内病原体生存而表现出致病性。粘附是成功入侵的关键先决条件，是由支原体表面粘附素与宿主细胞膜上的特定受体之间的相互作用协调的。侵袭在很大程度上依赖于网格蛋白和细胞膜穴介导的内化，伴随着多种激活的激酶、细胞骨架重排和无数的形态改变，例如膜内陷、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，它们就会在囊泡、细胞质、核周区域和细胞核中建立弹性庇护所，其中特定的环境条件有利于长期生存。尽管溶酶体降解和自噬可以消除大多数入侵的支原体，但一些活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。这篇综述探讨了支原体侵入宿主细胞并维持其难以捉摸的生存的复杂机制，目的是强调根除这种神秘细菌的挑战。