Summary Staphyllococcus aureus‐induced infections often result in high mortality and permanent joint destruction, despite treatment with antibiotics. IL‐10 is typically regarded as an anti‐inflammatory cytokine because it promotes a T helper cell type 2 response, and subsequently down‐regulates cell mediated immune functions. To investigate the role of IL‐10 in S. aureus‐induced arthritis and sepsis, Balb/c mice, intact or defective with respect to IL‐10 gene were intravenously inoculated with bacteria. IL‐10–/– mice develop a more frequent and destructive arthritis compared to their congeneic controls. The mechanisms regulating such outcome may be due not only to the anti‐inflammatory properties of IL‐10 but also, directly or indirectly, to antibacterial features of this molecule. Indeed, inoculation of staphylococci to IL‐10–/– mice resulted in higher bacterial load in blood and kidneys compared to congeneic controls. Altogether our data indicate that IL‐10 is essential for efficient elimination of bacteria and thereby for protection against septic arthritis.

SummaryMice deficient for the inhibitory G protein subunit a 2 (G a i2 -/-) spontaneously develop a progressive inflammatory bowel disease resembling ulcerative colitis, and have a T helper 1 (Th1)-dominated immune response prior to onset of colitis, which is further augmented after the onset of disease. The present study was performed to investigate whether the G a i2 -/-mice were able to down-regulate the Th1-dominated inflammatory mucosal immune response and/or induce an anti-inflammatory Th2/T regulatory response and thereby diminish the severity of colitis following treatment with acellular Bordetella pertussis vaccine . The acellular vaccine against B. pertussis , the causative agent of whooping cough, has been demonstrated to induce a Th2-mediated response in both man and mice. We therefore treated G a i2

The increased serum concentrations of IL-18 and IL-1Ra in established diseases are suggested as markers of ongoing colitis. Interestingly, the significantly increased serum concentration of IL-1Ra in pre-colitic mice is found to be an early marker of disease progression.