6533b7dafe1ef96bd126e202

RESEARCH PRODUCT

Subclinical gut inflammation in ankylosing spondylitis

Aroldo RizzoFrancesco CicciaGiovanni Triolo

subject

0301 basic medicineAnkylosing spondylitis; Gut inflammation; Innate lymphoid cells; Interleukin-17; Interleukin-23; Adaptive Immunity; Animals; Cytokines; Disease Models Animal; Dysbiosis; Gastrointestinal Microbiome; Humans; Immunity Innate; Inflammation; Inflammatory Bowel Diseases; Intestines; Macrophages; Mice; Spondylitis Ankylosing; Rheumatology; Medicine (all)MacrophageAdaptive ImmunityInterleukin-23Inflammatory bowel diseaseGastroenterologyMiceInterleukin 23InnateMedicineSubclinical infectionMedicine (all)Interleukin-17digestive oral and skin physiologyInnate lymphoid cellIntestineIntestinesCytokinesmedicine.symptomHumanAnkylosingmedicine.medical_specialtyDisease ModelInflammationdigestive system03 medical and health sciencesRheumatologyInternal medicineInnate lymphoid cellAnimalsHumansSpondylitis AnkylosingCytokineSpondylitisGut inflammationSpondylitiInflammationAnkylosing spondylitisAnimalbusiness.industryMacrophagesInflammatory Bowel DiseaseImmunityInflammatory Bowel Diseasesmedicine.diseaseImmunity InnateDysbiosiGastrointestinal MicrobiomeAnkylosing spondylitiDisease Models Animal030104 developmental biologyDysbiosisbusinessDysbiosis

description

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.

https://doi.org/10.1097/bor.0000000000000239