Th1/Th17-mediated Immunity and Protection from Peripheral Neuropathy in Wildtype and IL10 BALB/c Mice Infected with a Guillain-Barré Syndrome-associated Strain.

is an important cause of bacterial gastroenteritis worldwide and is linked to Guillain-Barré syndrome (GBS), a debilitating postinfectious polyneuropathy. The immunopathogenesis of GBS involves the generation of antibodies that are cross reactive to lipooligosaccharide and structurally similar peripheral nerve gangliosides. Both the infecting strain and host factors contribute to GBS development. GBS pathogenesis is associated with Th2-mediated responses in patients. Moreover, induction of IgG1 antiganglioside antibodies in association with colonic Th2-mediated immune responses has been reported in -infected C57BL/6 IL10 mice at 4 to 6 wk after infection. We hypothesized that, due to their Th2 immunologic bias, BALB/c mice would develop autoantibodies and signs of peripheral neuropathy after infection with a GBS patient-derived strain of (strain 260.94). WT and IL10 BALB/c mice were orally inoculated with 260.94, phenotyped weekly for neurologic deficits, and euthanized after 5 wk. Immune responses were assessed as -specific and antiganglioside antibodies in plasma and cytokine production and histologic lesions in the proximal colon. Peripheral nerve lesions were assessed in dorsal root ganglia and their afferent nerve fibers by scoring immunohistochemically labeled macrophages through morphometry. 260.94 stably colonized both WT and IL10 mice and induced systemic Th1/Th17-mediated immune responses with significant increases in -specific IgG2a, IgG2b, and IgG3 plasma antibodies. However, 260.94 did not induce IgG1 antiganglioside antibodies, colitis, or neurologic deficits or peripheral nerve lesions in WT or IL10 mice. Both WT and IL10 BALB/c mice showed relative protection from development of Th2-mediated immunity and antiganglioside antibodies as compared with C57BL/6 IL10 mice. Therefore, BALB/c mice infected with 260.94 are not an effective disease model but provide the opportunity to study the role of immune mechanisms and host genetic background in the susceptibility to post infectious GBS.