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      Mechanism of M-cell differentiation accelerated by proliferation of indigenous bacteria in rat Peyer’s patches

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          Abstract

          The mechanism by which indigenous bacteria on the follicle-associated epithelium (FAE) of lymphatic follicles (LFs) accelerate the differentiation of microvillous columnar epithelial cells (MV) into M-cells was immunohistochemically investigated in rat Peyer’s patches. The results showed that the number of Toll-like receptor (TLR) -4 + M-cells was greater in the FAE with expansion of bacterial colonies (LFs with bacterial colonies on the FAE: b-LF) than the FAE without expansion of bacterial colonies (nb-LF). TLR-4 was also expressed in the striated borders of MV upstream next to M-cells in the FAE of the b-LF. TLR-4 + vesicles were frequently detected in the cytoplasms of MV with TLR-4 + striated borders upstream next to TLR-4 + M-cells in the FAE of b-LF. These findings suggest that TLR-4 + MV take up TLR-4 ligands and differentiate into M-cells in the b-LF. Neither the distribution of RANK nor that of RANKL was coincident with that of M-cells in the b-LF. Moreover, RANK, but not RANKL, was expressed in intestinal villi, whereas cleaved caspase-3 was immunonegative in the MV and M-cells of the FAE, unlike in villous epithelial cells. Therefore, RANK/RANKL signaling in the LF might contribute to the down-regulation of epithelial apoptosis to facilitate the differentiation of MV into M-cells in rat Peyer’s patches.

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          Aberrant expansion of segmented filamentous bacteria in IgA-deficient gut.

          Keiichiro Suzuki, Bob Meek, Yasuko Doi … (2004)
          The mechanism to maintain homeostasis of the gut microbiota remains largely unknown despite its critical role in the body defense. In the intestines of mice with deficiency of activation-induced cytidine deaminase (AID), the absence of hypermutated IgA is partially compensated for by the presence of large amounts of unmutated IgM and normal expression levels of defensins and angiogenins. We show here a predominant and persistent expansion of segmented filamentous bacteria throughout the small intestine of AID(-/-) mice. Reconstitution of lamina propria IgA production in AID(-/-) mice recovered the normal composition of gut flora and abolished the local and systemic activation of the immune system. The results indicate that secretions of IgAs rather than innate defense peptides are critical to regulation of commensal bacterial flora and that the segmented filamentous bacteria antigens are strong stimuli of the mucosal immune system.
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            Critical roles of activation-induced cytidine deaminase in the homeostasis of gut flora.

            Sidonia Fagarasan, Masamichi Muramatsu, Keiichiro Suzuki … (2002)
            Activation-induced cytidine deaminase (AID) plays an essential role in class switch recombination (CSR) and somatic hypermutation (SHM) of immunoglobulin genes. We report here that deficiency in AID results in the development of hyperplasia of isolated lymphoid follicles (ILFs) associated with a 100-fold expansion of anaerobic flora in the small intestine. Reduction of bacterial flora by antibiotic treatment of AID-/- mice abolished ILF hyperplasia as well as the germinal center enlargement seen in secondary lymphoid tissues. Because an inability to switch to immunoglobulin A on its own does not lead to a similar phenotype, these results suggest that SHM of ILF B cells plays a critical role in regulating intestinal microflora.
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              Caspase 3 activity is required for skeletal muscle differentiation.

              Pasan Fernando, Ruth S. Slack, Jeffrey F. Kelly … (2002)
              The cellular alterations associated with skeletal muscle differentiation share a high degree of similarity with key phenotypic changes usually ascribed to apoptosis. For example, actin fiber disassembly/reorganization is a conserved feature of both apoptosis and differentiating myoblasts and the conserved muscle contractile protein, myosin light chain kinase, is required for the apoptotic feature of membrane blebbing. As such, these observations suggest that the induction of differentiation and apoptosis in the myogenic lineage may use overlapping cellular mechanisms. Here, we report that skeletal muscle differentiation depends on the activity of the key apoptotic protease, caspase 3. Peptide inhibition of caspase 3 activity or homologous deletion of caspase 3 leads to dramatic reduction in both myotube/myofiber formation and expression of muscle-specific proteins. Subsequently, we have identified Mammalian Sterile Twenty-like kinase as a crucial caspase 3 effector in this cellular process. Mammalian Sterile Twenty-like kinase is cleavage-activated by caspase 3, and restoration of this truncated kinase in caspase 3 null myoblasts restores the differentiation phenotype. Taken together, these results confirm a unique and unanticipated role for a caspase 3-mediated signal cascade in the promotion of myogenesis.
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                Author and article information

                Journal
                Journal ID (nlm-ta): J Vet Med Sci
                Journal ID (iso-abbrev): J. Vet. Med. Sci
                Journal ID (publisher-id): JVMS
                Title: The Journal of Veterinary Medical Science
                Publisher: The Japanese Society of Veterinary Science
                ISSN (Print): 0916-7250
                ISSN (Electronic): 1347-7439
                Publication date (Electronic): 08 October 2017
                Publication date (Print): November 2017
                Volume: 79
                Issue: 11
                Pages: 1826-1835
                Affiliations
                [1) ]Laboratory of Histophysiology, Department of Bioresource Science, Graduate School of Agricultural Science, Kobe University, 1-1 Rokkodai-cho, Nada-ku, Kobe, Hyogo 657-8501, Japan
                [2) ]Laboratory of Molecular Morphology, Department of Bioresource Science, Graduate School of Agricultural Science, Kobe University, 1-1 Rokkodai-cho, Nada-ku, Kobe, Hyogo 657-8501, Japan
                [3) ]Center for Collaborative Research and Technology Development, Kobe University, 1-1 Rokkodai-cho, Nada-ku, Kobe, Hyogo 657-8501, Japan
                [4) ]Laboratory of Microbiology and Immunology, Department of Bioresource Science, Graduate School of Agricultural Science, Kobe University, 1-1 Rokkodai-cho, Nada-ku, Kobe, Hyogo 657-8501, Japan
                Author notes
                [* ]Correspondence to: Kitagawa, H.: hkitagaw@ 123456kobe-u.ac.jp
                Article
                Publisher ID: 17-0470
                DOI: 10.1292/jvms.17-0470
                PMC ID: 5709560
                PubMed ID: 28993550
                SO-VID: 45acc170-7ee4-49cf-b670-27d2c0262920
                Copyright © ©2017 The Japanese Society of Veterinary Science
                License:

                This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial No Derivatives (by-nc-nd) License. (CC-BY-NC-ND 4.0: https://creativecommons.org/licenses/by-nc-nd/4.0/)

                History
                Date received : 21 August 2017
                Date accepted : 24 September 2017
                Categories
                Subject: Anatomy
                Subject: Full Paper

                Keywords: immunohistochemistry,indigenous bacteria,m-cell differentiation,peyer’s patch,rat
                Data availability:
                Keywords: immunohistochemistry, indigenous bacteria, m-cell differentiation, peyer’s patch, rat

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