Unveiling the stealthy tactics: mycoplasma’s immune evasion strategies

Abstract

Mycoplasmas, the smallest known self-replicating organisms, possess a simple structure, lack a cell wall, and have limited metabolic pathways. They are responsible for causing acute or chronic infections in humans and animals, with a significant number of species exhibiting pathogenicity. Although the innate and adaptive immune responses can effectively combat this pathogen, mycoplasmas are capable of persisting in the host, indicating that the immune system fails to eliminate them completely. Recent studies have shed light on the intricate and sophisticated defense mechanisms developed by mycoplasmas during their long-term co-evolution with the host. These evasion strategies encompass various tactics, including invasion, biofilm formation, and modulation of immune responses, such as inhibition of immune cell activity, suppression of immune cell function, and resistance against immune molecules. Additionally, antigen variation and molecular mimicry are also crucial immune evasion strategies. This review comprehensively summarizes the evasion mechanisms employed by mycoplasmas, providing valuable insights into the pathogenesis of mycoplasma infections.

The complete genome sequence of unculturable Mycoplasma faucium obtained through clinical metagenomic next-generation sequencing

“…GAPDH has been implicated in adherence to host cells, invasion and modulation of the host immune response ( Wang et al., 2023a ). It can interact with host cell components and contribute to the bacteria’s ability to establish infection ( Wang et al., 2023b ).…”

Antagonistic effects of actin-specific toxins onSalmonellaTyphimurium invasion into mammalian cells

“…Other pathogens utilize the motoric function of actin polymerization for locomotion inside the host cell (e.g., Listeria 11,12 , Shigella 12 , Rickettsia 11,13 , Burkholderia 14 ). In contrast, many other effector proteins disrupt actin filaments to compromise the integrity of epithelial barriers, facilitate colonization, and disrupt the phagocytic activity of immune cells (e.g., Vibrio [15][16][17] , Mycoplasm 18 , enterohemorrhagic Escherichia coli (EHEC) 19,20 ). Therefore, we hypothesized that the effects of some pathogens may conflict with the mechanisms employed by other bacterial pathogens, resulting in indirect competition for common host targets such as actin cytoskeleton.…”