IL-23 favours outgrowth of spondyloarthritis-associated pathobionts and suppresses host support for homeostatic microbiota
Linda M Rehaume, Nicholas Matigian, Ahmed M Mehdi, Nancy Lachner, Kate L Bowerman, Joshua Daly, Kim-Anh Le Cao, Philip Hugenholtz, Ranjeny Thomas
ANNALS OF THE RHEUMATIC DISEASES | BMJ PUBLISHING GROUP | Published : 2019
OBJECTIVES: Certain gut bacterial families, including Bacteroidaceae, Porphyromonadaceae and Prevotellaceae, are increased in people suffering from spondyloarthropathy (SpA), a disease group associated with IL23R signalling variants. To understand the relationship between host interleukin (IL)-23 signalling and gut bacterial dysbiosis in SpA, we inhibited IL-23 in dysbiotic ZAP-70-mutant SKG mice that develop IL-23-dependent SpA-like arthritis, psoriasis-like skin inflammation and Crohn's-like ileitis in response to microbial beta 1,3-glucan (curdlan). METHODS: We treated SKG mice weekly with anti-IL-23 or isotype mAb for 3 weeks, rested them for 3 weeks, then administered curdlan or saline...View full abstract
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Awarded by NHMRC
The study was supported by NHMRC grant 1071822 and grants-in-aid from Arthritis Australia. RT was supported by Arthritis Queensland and NHMRC Research Fellowship. AMM was supported by JDRF Postdoctoral Fellowship. KALC was supported by NHMRC Career Development Fellowship and PH was supported by ARC Laureate Fellowship.