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Originally published online as doi:10.2353/ajpath.2008.070393 on February 7, 2008

Published online before print February 7, 2008
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(American Journal of Pathology. 2008;172:671-680.)
© 2008 American Society for Investigative Pathology
DOI: 10.2353/ajpath.2008.070393

Resistance of Chemokine Receptor 6-Deficient Mice to Yersinia Enterocolitica Infection

Evidence of Defective M-Cell Formation in Vivo

Sabine Westphal*, Andreas Lügering*, Julia von Wedel*, Christof von Eiff{dagger}, Christian Maaser*, Thomas Spahn*, Gerhard Heusipp{ddagger}, M. Alexander Schmidt{ddagger}, Hermann Herbst§, Ifor R. Williams, Wolfram Domschke* and Torsten Kucharzik*

From the Department of Medicine B,*and the Institutes of Medical Microbiology{dagger}and Infectiology,{ddagger}University of Muenster, Muenster, Germany; the Institute of Pathology,§Klinikum Neukoelln, Berlin, Germany; and the Department of Pathology and Laboratory Medicine,Emory University School of Medicine, Atlanta, Georgia

M cells, specialized cells within Peyer’s patches (PPs), are reduced in number in chemokine receptor 6 (CCR6)-deficient mice. The pathogenic microorganism Yersinia enterocolitica exploits M cells for the purpose of mucosal tissue invasion exclusively through PPs. The aim of this study was to evaluate the course of yersiniosis in CCR6-deficient mice and to investigate whether these mice might be used as an in vivo model to determine M-cell function. After oral challenge with Y. enterocolitica, control mice suffered from lethal septic infection whereas CCR6-deficient mice showed very limited symptoms of infection. Immunohistochemical analysis demonstrated PP invasion by Y. enterocolitica in control mice whereas no bacteria could be found in CCR6-deficient mice. In addition, a significant induction of proinflammatory cytokines could be found in control mice whereas proinflammatory cytokine levels in CCR6-deficient mice remained unchanged. In contrast, intraperitoneal infection resulted in severe systemic yersiniosis in both mouse groups. Abrogated oral Y. enterocolitica infection in CCR6-deficient mice demonstrates the importance of CCR6 expression in the physiological and pathological immune responses generated within PPs by influencing M-cell differentiation, underscoring the important role of M cells in the process of microbial uptake. CCR6-deficient mice may therefore represent a suitable model for the study of M-cell function in vivo.




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