Mycoplasma hominis surface and secreted antigens

Mycoplasma hominis surface and secreted antigens are a diverse group of proteins and lipoproteins that play essential roles in the survival, colonization, and pathogenicity of this cell-wall-less bacterium (Waites and Talkington, 2005, https://pubmed.ncbi.nlm.nih.gov/15908458/). Key surface antigens include the Variable Adherence-Associated (Vaa) protein, which mediates attachment to host cells, and the P120 and P120' proteins, which are involved in immune evasion through high genetic variability (Boesen et al., 2004, https://pubmed.ncbi.nlm.nih.gov/15383625/; Nyvold et al., 1997, https://pubmed.ncbi.nlm.nih.gov/9046668/). The Large Multiple-banded Protein (Lmp) family and the OppA protein also contribute to adhesion and biofilm formation (Ladefoged et al., 1996, https://pubmed.ncbi.nlm.nih.gov/8946244/). Secreted or surface-exposed enzymes like the MhoS nuclease and arginine deiminase (ADI) are critical for nutrient acquisition and evading the host's innate immune response, such as neutrophil extracellular traps (NETs) (Henrich et al., 2019, https://pubmed.ncbi.nlm.nih.gov/31665487/; Misawa et al., 1994, https://pubmed.ncbi.nlm.nih.gov/7990139/). These antigens are primary targets for the host's humoral immune response and are extensively studied as candidates for diagnostic assays and vaccine development. While current treatment for M. hominis infections relies on antibiotics like doxycycline and moxifloxacin that target intracellular processes, these surface antigens represent potential targets for novel immunotherapies, and ADI itself is being explored as a therapeutic agent (ADI-PEG20) for arginine-auxotrophic cancers (Feun et al., 2010, https://pubmed.ncbi.nlm.nih.gov/20194465/).

Other names

M. hominis surface proteinsMycoplasma hominis membrane antigensVariable adherence-associated protein (Vaa)P120 surface proteinLarge multiple-banded protein (Lmp) familyP80 lipoproteinOligopeptide permease A (OppA)MhoS nucleaseArginine deiminase (ADI)

Inhibition of bacterial protein synthesis by binding to the 30S or 50S ribosomal subunits (Tetracyclines, Lincosamides); Inhibition of DNA gyrase and topoisomerase IV to prevent DNA replication (Fluoroquinolones); Depletion of systemic arginine to starve arginine-auxotrophic cells (ADI-PEG20)