Cellular Tight Junctions Prevent Effective Campylobacter jejuni Invasion and Inflammatory Barrier Disruption Promoting Bacterial Invasion from Lateral Membrane in Polarized Intestinal Epithelial Cells

Hatayama, Sho; Shimohata, Takaaki; Amano, Sachie; Kido, Junko; Nguyen, Anh Quoc; Sato, Yuri; Kanda, Yuna; Tentaku, Aya; Fukushima, Shiho; Nakahashi, Mutsumi; Uebanso, Takashi; Mawatari, Kazuaki; Takahashi, Akira

doi:10.3389/fcimb.2018.00015

Cited by 18 publications

(15 citation statements)

References 60 publications

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“…These findings suggested that probiotic B. subtilis LF11 played a role on preventing cytokine-mediated gastrointestinal diseases. Previous studies have shown that proinflammatory cytokines including TNF-α mediate tight junction disruption, which increases the pathogen’s invasion process in epithelial cells ( Hatayama et al., 2018 ). In addition, it was noticed that the exclusion activity was always stronger than competition activity, suggesting that the supplementation with B. subtilis LF11 in diets was an effective way to prevent the Salmonella infection in poultry farming.…”

Section: Discussionmentioning

confidence: 99%

Probiotic Bacillus subtilis LF11 Protects Intestinal Epithelium Against Salmonella Infection

Zhang

et al. 2022

Front. Cell. Infect. Microbiol.

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Enteric diseases caused by Salmonella are prevalent in poultry farming. With the forbiddance of antibiotics in feedstuff industry, Bacillus subtilis (B. subtilis) preparation as antibiotic alternatives against Salmonella infection has gained increasing attention recently. However, the protection modes of B. subtilis against Salmonella infection in broilers are strain-specific. In this study, probiotic B. subtilis LF11 significantly reduced diarrhea and mortality of broilers caused by Salmonella braenderup (S. braenderup) in spite of no inhibition effect on it in vitro. Here, the intestinal epithelial cells NCM460 were incubated to explore the protection of B. subtilis LF11 on intestinal epithelium against Salmonella. The results revealed that B. subtilis LF11 showed obvious exclusion activity with the decrease of adhesion and invasion of S. braenderup to NCM460 cells, accordingly with the increase of NCM460 cell survival compared with S. braenderup challenge alone. Meanwhile, RT-PCR and Western blot proved that the gene transcription and expression levels of four tight junction proteins in NCM 460 cells were upregulated, which was further confirmed by immunofluorescence observation. Besides, B. subtilis LF11 downregulated the gene transcription levels of the proinflammatory cytokines IL-6, IL-8, and TNF-α induced by S. braenderup H9812. ELISA analysis also verified that B. subtilis LF11 reduced the IL-8 production significantly. In general, B. subtilis LF11 has the ability to protect the intestinal epithelium against Salmonella infection by reducing the Salmonella adhesion and invasion, enhancing the intestinal barrier and attenuating the enterocyte inflammatory responses, and has the potential as probiotics to prevent enteric diseases in broilers.

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Section: Discussionmentioning

confidence: 99%

Probiotic Bacillus subtilis LF11 Protects Intestinal Epithelium Against Salmonella Infection

Zhang

et al. 2022

Front. Cell. Infect. Microbiol.

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“…We also determined the subcellular localization of claudin-1 and claudin-2 and found that ETEC infection induces the cytoplasmic distribution of claudin-2, but not claudin-1. Claudin-1 are exclusively located in the junctional area of IPEC-J2 cells following infection with a variety of porcine ETEC strains and porcine epidemic diarrhea virus [40, 41], indicating the essential role of this TJ protein in preventing intestinal pathogens to enter the paracellular space and invade the host [42]. Claudin-2 has been shown to form a paracellular channel for small ions and water and its upregulation is linked to leaky epithelial barriers and diarrhea [43, 44].…”

Section: Discussionmentioning

confidence: 99%

Toll-like receptor 5-mediated IL-17C expression in intestinal epithelial cells enhances epithelial host defense against F4+ ETEC infection

Luo

Zhang

et al. 2019

Vet Res

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Enterotoxigenic Escherichia coli (ETEC) are an important cause of post-weaning diarrhea (PWD) in piglets. The IL-17 cytokine family is well known to play important roles in the host defense against bacterial infections at the mucosa. Previously, we reported the potential role of IL-17A in clearing an ETEC infection in piglets. IL-17C, another member of the IL-17 family, is highly expressed in the intestinal epithelium, however, its role during an ETEC infection is still unclear. In this study, we demonstrate that F4 + ETEC induce IL-17C mRNA and protein expression in intestinal tissues as well as in porcine intestinal epithelial cells (IPEC-J2). This IL-17C production is largely dependent on TLR5 signaling in IPEC-J2 cells. Both F4 + ETEC infection and exogenous IL-17C increased the expression of antimicrobial peptides and tight junction proteins, such as porcine beta-defensin (pBD)-2, claudin-1, claudin-2 and occludin in IPEC-J2 cells. Taken together, our data demonstrate that TLR5-mediated IL-17C expression in intestinal epithelial cells enhances mucosal host defense responses in a unique autocrine/paracrine manner in the intestinal epithelium against ETEC infection. Electronic supplementary material The online version of this article (10.1186/s13567-019-0665-8) contains supplementary material, which is available to authorized users.

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“…In S. aureus, fnbA and fnbB single mutants show no significant reduction in adhesion to FN [46], but both FNBPs are required for severe disease in mice [56]. Compared with other known and putative C. jejuni adhesins, a distinguishing feature of the CadF and FlpA proteins is that they promote cellular invasion by binding to FN bound to α 5 β 1 integrins on the basolateral surface of a cell [57][58][59]. However, in the early 1990s, it was also reported that C. jejuni invasion, but not cell adherence, was significantly reduced in the presence of chloramphenicol, a selective inhibitor of bacterial protein synthesis [60].…”

Section: Discussionmentioning

confidence: 99%

Molecular Dissection of the Campylobacter jejuni CadF and FlpA Virulence Proteins in Binding to Host Cell Fibronectin

et al. 2020

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Campylobacter jejuni, a zoonotic pathogen that frequently colonizes poultry, possesses two Microbial Surface Components Recognizing Adhesive Matrix Molecule(s) (MSCRAMMs) termed CadF and FlpA that bind to the glycoprotein fibronectin (FN). Previous to this study, it was not known whether the CadF and FlpA proteins were functionally redundant or if both were required to potentiate host cell binding and signaling processes. We addressed these questions by generating a complete repertoire of cadF and flpA mutants and complemented isolates, and performing multiple phenotypic assays. Both CadF and FlpA were found to be necessary for the maximal binding of C. jejuni to FN and to host cells. In addition, both CadF and FlpA are required for the delivery of the C. jejuni Cia effector proteins into the cytosol of host target cells, which in turn activates the MAPK signaling pathway (Erk 1/2) that is required for the C. jejuni invasion of host cells. These data demonstrate the non-redundant and bi-functional nature of these two C. jejuni FN-binding proteins. Taken together, the C. jejuni CadF and FlpA adhesins facilitate the binding of C. jejuni to the host cells, permit delivery of effector proteins into the cytosol of a host target cell, and aid in the rewiring of host cell signaling pathways to alter host cell behavior.

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Cellular Tight Junctions Prevent Effective Campylobacter jejuni Invasion and Inflammatory Barrier Disruption Promoting Bacterial Invasion from Lateral Membrane in Polarized Intestinal Epithelial Cells

Cited by 18 publications

References 60 publications

Probiotic Bacillus subtilis LF11 Protects Intestinal Epithelium Against Salmonella Infection

Probiotic Bacillus subtilis LF11 Protects Intestinal Epithelium Against Salmonella Infection

Toll-like receptor 5-mediated IL-17C expression in intestinal epithelial cells enhances epithelial host defense against F4+ ETEC infection

Molecular Dissection of the Campylobacter jejuni CadF and FlpA Virulence Proteins in Binding to Host Cell Fibronectin

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