Abstract Title:

Heat-killed probiotic regulates the body's regulatory immunity to attenuate subsequent experimental autoimmune arthritis.

Abstract Source:

Immunol Lett. 2019 Oct 20. Epub 2019 Oct 20. PMID: 31644891

Abstract Author(s):

Hai Jia, Shipu Ren, Xia Wang

Article Affiliation:

Hai Jia


Administration of inactivated probiotics has been proved to enhance host immunity. Herein, we aim to explore their potential in modulating systemic autoimmune disorders. The bovine type II collagen (CII)-induced arthritis (CIA) and CII antibody-induced arthritis (CAIA) mice model was used in this study. Heat-killed Lactobacillus reuteri (h-L. reuteri) was administered before or after the induction of CIA. The results indicated that the severity of CIA was alleviated and the prevalence of CIA was decreased in the mice pre-treated with h-L. reuteri. Using enzyme-linked immunosorbent assays, we found that decreased serum CII-specific IgG antibody IL-6 and CXCL1 but the increased level of IL-10 was found in h-L. reuteri-treated cohort. Moreover, h-L. reuteri treatment decreased the severity and incidence of arthritis in the CAIA model which is associated with a early decrease of IL-6. Systematic supplement of exogenous IL-6 reversed h-L. reuteri-induced CIA suppression. For regulatory immune responses, the frequency of Tregs and CD4+IL-10+ cells was increased in the draining lymph of joint of h-L. reuteri-treated mice after second immunization. Parallelly, we found that if CIA was induced, CD103+ dendritic cells in mesenteric lymph nodes andα4β7+ Tregs in the spleen were increased in h-L. reuteri-treated mice, suggesting h-L. reuteri might affect the peripheral migration of Tregs to modulating CIA. Finally, the mice with progressive CIA were treated with h-L. reuteri after the second immunization. No alleviation of CIA severity, as well as an increase of splenic α4β7+ Tregs, was observed in these mice. This study indicates that pre-administration of h-L. reuteri can alleviate the CIA in mice and may serve as a promising strategy for autoimmune disease prevention.

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