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. 2023 Aug 9;14:1228754. doi: 10.3389/fimmu.2023.1228754

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Copyright © 2023 Luo, Chen, Xie, Liu, Jiang and Yu

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Protection of the integrity of intestinal mucosal barrier. Administration of both L. reuteri D8 and L. reuteri 22 increased the number of ISCs, Lgr5⁺ cells, and promoted the proliferation of IECs by activating the Wnt/β-catenin pathway. L. reuteri 22 inhibited Notch signaling pathway and induced the differentiation of ISCs into Muc-2-highly expressing goblet cells, whereas L. reuteri D8 induced the differentiation of ISCs into Paneth cells. Both L. reuteri DSM17938 and 1563F upregulated the expression of E-cadherin and TJs in infected IECs and competitively inhibited bacterial binding to TJs, thus inhibiting the increased infection-induced intestinal permeability and protecting intestinal barrier function. Upregulation of the expression of TJs in intestinal epithelium can be achieved by inhibiting the TLR4/MyD88 signal transduction pathway and downregulating the MLCK pathway. ISCs, intestinal stem cells; mucin-2, Muc-2; IECs, intestinal epithelial cells; TJs, tight junctions; TLR4, Toll-like receptor 4; MyD88, myeloid differentiation factor 88; MLCK, myosin light chain kinase.