Contrasting immune responses mediate Campylobacter jejuni-induced colitis and autoimmunity

Campylobacter jejuni is a leading cause of foodborne enteritis that has been linked to the autoimmune neuropathy, Guillain Barre ' syndrome (GBS). C57BL/6 interleukin (IL)-10_/_ and congenic IL-10 -/- mice serve as C. jejuni colonization and colitis models, respectively, but a mouse model forGBSis lacking. Wedemonstrate that IL-10 -/- mice infected with a C. jejuni colitogenic human isolate had significantly upregulated type 1 and 17 but not type 2 cytokines in the colon coincident with infiltration of phagocytes, T cells and innate lymphoid cells (ILCs). Both ILC and T cells participated in interferon-c (IFN-c), IL-17, and IL-22 upregulation but in a time-and organ-specific manner. Tcells were, however, necessary for colitis as mice depleted of Thy-1 cells were protected while neither Rag1 -/- nor IL-10R blocked Rag1 -/- mice developed colitis after infection. Depleting IFN-c, IL-17, or both significantly ameliorated colitis and drove colonic responses toward type 2 cytokine and antibody induction. In contrast, C. jejuni GBS patient strains induced mild colitis associated with blunted type 1/17 but enhanced type 2 responses. Moreover, the type 2 but not type 1/17 antibodies cross-reacted with peripheral nerve gangliosides demonstrating autoimmunity.