Analysis of enterotoxigenic effect of Staphylococcus aureus and Staphylococcus epidermidis enterotoxins C and L on mice

Pathogenic properties of orthologues to S. aureus staphylococcal enterotoxin C (SEC) and staphylococcal enterotoxin L (SEL) produced by S. epidermidis are largely unexplored. We assessed the enteropathogenic effects of S. epidermidis SEC(epi )and SEL(epi )and S. aureus SEC3 and SEL after oral administration to Balb/c mice. Intestinal sections from SE-treated mice were analyzed histopathologically. The T cell lineage markers (alpha beta and gamma delta TCR CD3, CD4, CD8), T-cell activation marker CD69 and proliferation-related marker CD71 were assessed in intraepithelial lymphocytes (IEL), mesenteric lymph nodes (MLN) and spleens (SPL). Serum concentrations of SEC and SEL were determined. Ortologous S. epidermidis and S. aureus SEs exerted a number of common histopathological changes in the mouse gut. Atrophy, generation of villi gap and edema of the villi were the most prominent effects of SE treatment observed in mouse gut sections. The most marked effect of ortologous S. epidermidis and S. aureus SEs on the number of goblet cells, crypt depth and villi height was noted in the mice duodenum and jejunum. We indicate early changes of TCR alpha beta CD4(-)CD8a(+) T and TCR alpha beta CD4(+)CD8a(+) T cells in response to both S. aureus and S. epidermidis SEs. Upon the treatment with SEs, markers of T cell activation and proliferation were upregulated in both alpha beta and gamma 8 T cell populations derived from IEL and MLN. We demonstrated that S. epidermidis-encoded SEs applied via oral route exert pathological changes in mice gut similarly to S. aureus-encoded SEs. For the first time we indicated that SEL co-produced together with SEC by both S. aureus and S. epidermidis induces some elements of mice gut immune response and contributes to gastrointestinal tract damage. Our results indicate the potential involvement of CoNS-encoded enterotoxins in the pathogenesis of SFP.

Automated summary

Orthologues of S. aureus and S. epidermidis produced similar pathological changes in the mouse gut, including villi atrophy, generation of villi gap, and villi edema. These toxins also affected T cell activation and proliferation in the gut.