An important mechanism by which immune responses could be controlled in the skin of mice is revealed in a report published online in Nature Immunology this week. This study offers possible new options for tackling serious drug resistant bacterial infections of the skin such as that caused by MRSA, bacteria that have been especially troublesome in hospitals.
Sandip Datta and colleagues looked at immune responses to drug-resistant Staphylococcus aureus - the most clinically significant bacterial pathogen of the skin and the causative agent of MRSA - and focused in particular on the role of the IL-20 family of cytokines. These signaling molecules are released by keratinocytes in the skin and have been implicated in psoriasis but have never been examined in the context of infection. The authors found that in mice and human skin samples, the IL-20 family cytokines were released in response to S. aureus infection and dampened other immune responses by blocking IL-1 production- a key factor required for controlling the bacteria. The action of the IL-20 family cytokines in the skin therefore exacerbated infection but on the flipside, blocking them improved the immune responses to S. aureus.