Abstract

Abstract It was characterized that the innate lymphoid cells (ILCs) are a group of immune cells closely associated with immune functions such as lymphoid organogenesis, tissue remodeling, antimicrobial immunity, and inflammation through cytokine-mediated cell regulation. ILC subsets can be categorized into three groups based on cytokine-secreting patterns. Group 1 ILCs secrete IFN-γ. Group 2 produces type 2 cytokines dependent on GATA-3. Group 3 represents all RORγt+ ILC subtypes secreting IL-17 and/or IL-22. In mucosal immunity, RORγt+ ILCs play an essential role in early protection against enteric pathogen infections, although its regulation by mucosal environment is unknown. In this study, we suggest that butyrate, one of commensal microbe-derived metabolites, as a modulator of PP ILCs, because it is known that butyrate treatment closely associated with the protection of bacterial infection or DSS-induced colitis. In order to understand the mechanism underlying the proposed role of butyrate, we monitored the expression pattern of each transcription factors and cytokines in PP ILCs after oral administration of sodium butyrate in SPF and antibiotics-treated mice. To understand the regulating activity of PP ILCs induced by butyrate in mucosal immunity, we try to understand the regulation of DSS colitis in the same mice. Collectively, this study suggests that regulation of ILCs by butyrate in gastrointestinal tract was closely associated with maintaining mucosal homeostasis.

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