PubMed · 3548533
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J G Bartlett. 1986. New intestinal pathogens.. https://pubmed.ncbi.nlm.nih.gov/3548533/
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Guillain-Barré syndrome (GBS), an autoimmune disease of the peripheral nervous system, is associated with antecedent Campylobacter jejuni infection. GM and KM allotypes--genetic markers of immunoglobulin gamma and kappa chains, respectively--are implicated in the etiopathogenesis of several autoimmune diseases. To determine if GM/KM phenotypes are associated with GBS and influence antibody responses to C. jejuni and to GM1 and GD1a gangliosides, 72 Japanese GBS patients and 73 controls were allotyped for several GM and KM markers. Sera from patients were characterized for antibodies to C. jejuni, GM1, and GD1a. The distribution of KM phenotypes was significantly different in patients with anti-GD1a ganglioside antibodies from those who lacked these antibodies (P=0.029). No other significant associations were found. These results suggest that KM allotypes are not risk factors for developing GBS, but contribute significantly to the generation of autoimmune responses to GD1a ganglioside in patients with this disease.
Campylobacter jejuni is the predominant cause of antecedent infection in Guillain-Barré syndrome (GBS) or Miller Fisher syndrome (MFS). C. jejuni probably triggers GBS or MFS through molecular mimicry between bacterial sialylated lipo-oligosaccharides (LOS) and gangliosides in peripheral nerve tissue. We investigated whether co-infections with multiple C. jejuni strains occur in GBS or MFS patients and we further characterized these strains. PFGE analysis of 83 C. jejuni isolates from single primary colonies from stool cultures of 13 patients with GBS or MFS revealed co-infection with two different strains in one patient (8%). We showed that only strain GB5.1 contained an LOS biosynthesis gene locus that is associated with neuropathy. The patient serum strongly reacted with the LOS of strain GB5.1 and not with the LOS of strain GB5.2. Mass spectrometry revealed that both strains expressed a non-sialylated outer core structure in their LOS. The patient serum contained anti-asialo-GM2 antibodies that cross-reacted with the LOS of strain GB5.1. This study demonstrates that co-infection with multiple C. jejuni strains occurs in GBS patients. Consequently, not all C. jejuni strains isolated from the faeces of a GBS patient are involved in the pathogenesis of GBS per se. Furthermore, this is the first report in which cross-reactivity of antibodies to asialo-GM2 and to the LOS of a C. jejuni strain from a GBS patient has been demonstrated. This finding suggests that molecular mimicry with non-sialylated structures may also be involved in the pathogenesis of GBS.
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