Course of Yersinia enterocolitica infection is dramatically improved in CCR6 deficient mice ‐ a new in vivo model for M cell function?

Introduction M cells are specialized cells within the follicle associated epithelium (FAE) of Peyer's patches (PP). We could recently demonstrate that CCR6‐deficient mice lack M cells, the “gatekeepers” of the mucosal immune system. Yersinia enterocolitica selectively exploit M cells to invade mucosal tissues and spread systemically. Due to involvement of M cell system the Yersinia enterocolitica infection model appears particularly interesting in studying M cell integrity and function in CCR6 KO mice. Results After oral application of Y. enterocolitica , CCR6‐deficient mice showed no clinical symptoms of infection, whereas wildtype (wt) mice suffered from septic infection. 7 days post infection, Yersinia could be found in PP isolated from wt mice but not in KO mice. No bacterial invasion could be observed in spleens. In addition, a significantly elevated level of TNFα RNA expression within PP of wt mice could be evaluated. Conclusions The interaction of CCR6 with its ligand Mip3α is essential for the development of PP and M cells. Deletion of CCR6 causes inhibition of M cell differentiation and consecutively decreased infectious potential of Y. enterocolitica . The CCR6 knockout mouse model represents a suitable instrument to characterize function of M cells in vivo . Supported by grants from the Deutsche Forschungsgemeinschaft (LU816/2‐1)