[i]Staphylococcus aureus[/i] phenol-soluble modulins impair interleukin expression in bovine mammary epithelial cells.
Résumé
While the role of many cytokines during infection is revealed, the implication of several recently discovered cytokines during infection is not completely understood. The involvement of currently described interleukin-32 (IL-32) in infectious mastitis (an inflammation of the mammary gland), caused by two prevalent mastitis pathogens, Staphylococcus aureus (S. aureus) and Escherichia coli (E. coli) , was not investigated so far.
We determined expression of IL-32, IL-6 and IL-8 in S. aureus- as compared to E.coli-infected bovine mammary gland epithelial cells. Using live bacteria we found that in S. aureus-infected cells, induction of IL-6 and IL-8 expression was less pronounced than in E. coli-infected cells. Notably, IL-32 expression was decreased in S. aureus-infected cells, while it was increased in E. coli-infected cells. IL-32 expression in E. coli- and S. aureus-infected udder tissue resembles in vitro responses.
We identified the staphylococcal phenol-soluble modulin (PSM) peptides as key contributors to these effects, as IL-32, IL-6 and IL-8 expression by epithelial cells exposed to psm mutant strains was significantly increased as compared to cells exposed to the isogenic S. aureus wild-type strain, indicating that PSMs inhibit the production of these interleukins. The use of genetically complemented strains confirmed this observation. Inasmuch as the decreased expression of IL-32, which is involved in dendritic cell maturation, impairs immune responses, our results support a PSM-dependent mechanism that allows for the development of chronic S aureus-related mastitis.