Francesco Ciccia1, Aroldo Rizzo, Giovanni Triolo. 1. aDipartimento Biomedico di Medicina Interna e Specialistica, Sezione di Reumatologia, Università degli Studi di Palermo bDipartimento di Oncoematologia, Azienda Ospedaliera Ospedali riuniti Villa Sofia-Cervello, Palermo, Italy.
Abstract
PURPOSE OF REVIEW: Subclinical gut inflammation has been described in a significant proportion of patients with ankylosing spondylitis (AS), up to 10% of them developing it during the time of clinically overt inflammatory bowel disease. Histologic, immunologic, and intestinal microbiota alterations characterize the AS gut. RECENT FINDINGS: Microbial dysbiosis as well as alterations of innate immune responses have been demonstrated in the gut of AS. Furthermore, a growing body of evidence suggests that the gut of AS patients may be actively involved in the pathogenesis of AS through the production of proinflammatory cytokines, such as IL-23p19, and the differentiation of potentially pathogenic innate lymphoid cells producing IL-22 and IL-17. Finally, a strong correlation between the presence of subclinical gut inflammation and the degree of spine inflammation have been also proved in AS. SUMMARY: Subclinical gut inflammation and innate immune responses in AS may be considered a possible consequence of microbial dysbiosis. Relationships between cause and effect remain, however, to be answered.
PURPOSE OF REVIEW: Subclinical gut inflammation has been described in a significant proportion of patients with ankylosing spondylitis (AS), up to 10% of them developing it during the time of clinically overt inflammatory bowel disease. Histologic, immunologic, and intestinal microbiota alterations characterize the AS gut. RECENT FINDINGS:Microbial dysbiosis as well as alterations of innate immune responses have been demonstrated in the gut of AS. Furthermore, a growing body of evidence suggests that the gut of AS patients may be actively involved in the pathogenesis of AS through the production of proinflammatory cytokines, such as IL-23p19, and the differentiation of potentially pathogenic innate lymphoid cells producing IL-22 and IL-17. Finally, a strong correlation between the presence of subclinical gut inflammation and the degree of spine inflammation have been also proved in AS. SUMMARY: Subclinical gut inflammation and innate immune responses in AS may be considered a possible consequence of microbial dysbiosis. Relationships between cause and effect remain, however, to be answered.
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