Clostridium difficile
Clostridium difficile
As an infectious diseases specialist, Dr. Petri encounters C. difficile colitis nearly every day on the clinical service. We therefore asked if the insights that our lab was gaining into the pathogenesis of E. histolytica infectious colitis would be enlightening for this other infectious form of colitis. The first discovery was that the leptin receptor mutation (Q223R) that had such a striking impact on susceptibility to amebic colitis had a similar effect on C. difficile colitis. We hypothesized that leptin affords protection during C. difficile colitis by enhancing mucosal inflammation acutely and by promoting healing during recovery. We are pursuing this lead in human and mouse studies that have shown that IL-23 mediated inflammation is disease-enhancing and IL-25 protective. We have identified the role of eosinophils in mediating IL-25 protection and conversely C. difficile toxins A, B and binary toxin in mediating disease.