Staphylococcus aureus Releases Proinflammatory Membrane Vesicles To Resist Antimicrobial Fatty Acids.

摘要: Staphylococcus aureus is a major pathogen, which colonizes one in three otherwise healthy humans. This significant spread of S. largely due to its ability circumvent innate immune responses, including antimicrobial fatty acids (AFAs) on the skin and nasal secretions. In response AFAs, swiftly induces resistance mechanisms, have yet be completely elucidated. Here, we identify membrane vesicle (MV) release as strategy used by sequester host-specific AFAs. MVs protect against wide array Strikingly, beside MV production, modulates composition upon exposure purified from bacteria grown presence linoleic acid display distinct protein content are enriched lipoproteins, strongly activate Toll-like receptor 2 (TLR2). Cumulatively, our findings reveal protective capacities counteracted an increased TLR2-mediated response.IMPORTANCE The nares humans colonized these environments, arguably all mucosal surfaces, encounter with properties. Our study uncovers that releases vesicles (MVs) act decoys bacterium (AFAs). AFA-neutralizing effects were neither strain specific nor restricted particular AFA. Hence, may represent "public goods" playing overlooked role shaping bacterial communities AFA-rich environments such nose. Intriguingly, addition biogenesis, lipoproteins. These stimulate immunity via inflammation, helps fight infections, exacerbate inflammatory disorders like atopic dermatitis. highlights intricate responses preventing infections colonizing bacteria.