Autor(es): Phongsisay Vongsavanh,Hara Hiromitsu,Fujimoto Shuji

Resumo: Campylobacter jejuni causes gastroenteritis and autoimmune neuropathy Guillain-Barré syndrome. The mechanism by which C. jejuni infection results in such the hyperimmunity is not completely understood. Host immunity plays an important role in the disease pathogenesis; however, little is known how immune system recognizes this human pathogen. In this study, we report that Toll-like receptors recognize distinct proteinase K-resistant glycoconjugates in C. jejuni and Escherichia coli. Lipopolysaccharide is solely proteinase-resistant glycoconjugate in E. coli. In contrast, C. jejuni possesses at least five different components that are resistant to proteinase digestion and are capable of inducing NF-?B activation through TLR2 and TLR4. Possession of multiple activators of Toll-like receptors may be the unique strategy of C. jejuni to trigger hyperimmunity.

Palavras-Chave: Campylobacter jejuni; Inflammation; Toll-like receptors

Imprenta: Molecular Immunology, v. 64, n. 1, p. 195-203, 2015

Identificador do objeto digital: 10.1016/j.molimm.2014.11.020

Descritores: Guillain-Barre Syndrome - Biosynthesis ; Guillain-Barre Syndrome - Cytopathology ; Guillain-Barre Syndrome - Pathogenesis ; Guillain-Barre Syndrome - Proteins ; Guillain-Barre Syndrome - Cytokines ; Guillain-Barre Syndrome - Inflammation ; Guillain-Barre Syndrome - Molecular screening ; Guillain-Barre Syndrome - Immunology

Data de publicação: 2015

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