Commensal microbiota modulates phenotypic characteristics and gene expression in the piglet intestine Peyer's patches. Bacteria

The gastrointestinal tract contains a complex microbial community.Peyer's patches (PPs), an inducible site of intestinal lymphoid tissue, are the main source of intestinal IgA production.However, little is known about the molecular mechanism of host PPs-microbiota interactions.Here, we analyzed phenotypic-to-transcriptome changes in intestine PPs of germ-free (GF) and specific pathogen-free (SPF) piglets (respectively reared in the absence and presence of commensal microbiota) to elucidate the role of commensal microbiota in shaping host intestine mucosal immunity.Analysis of anatomical and histological characteristics showed that commensal microbiota deficiency leads to hypoplasia of PPs, especially B and T cells. A total of 12,444 mRNAs was identified to be expressed in 12 ibraries,2,156 and 425 differentially expressed (DE) mRNAs were detected in JPPs and IPP (SPF vs. GF), respectively.The shared DE mRNAs of JPP and IPP are mainly involved in the basic physiological and metabolic processes, while the specific DE mRNAs are enriched in the regulation of immune cells in JPP and microbial responses and cellular immunity in IPP, respectively.Commensal microbiota significantly modulated the B cell function-related genes, including B cell activation/proliferation/differentiation/apoptosis, B cell receptor signaling, germinal center formation, IgA class switching, particularly in JPP.TLR4 pathway-related genes were induced in response to microbial colonization and in LPS/SCFA-treated B cells. We also detected 69 and 21 DE lncRNAs in JPP and IPP, respectively, then four one-to-one lncRNA-mRNA pairs were identified.These might represent key regulatory axes for host intestine mucosal immunity development during microbial colonization.Commensal microbiota affects tissue development and modulates gene expression in piglet intestine PPs, underscoring the importance of microbiota for host mucosal immunity.