4.6 Article

Weissella cibariaAttenuated LPS-Induced Dysfunction of Intestinal Epithelial Barrier in a Caco-2 Cell Monolayer Model

Journal

FRONTIERS IN MICROBIOLOGY
Volume 11, Issue -, Pages -

Publisher

FRONTIERS MEDIA SA
DOI: 10.3389/fmicb.2020.02039

Keywords

Weissella cibaria; tight junction; intestinal barrier; inflammatory response; probiotics

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Funding

  1. Certificate of China Postdoctoral Science Foundation [2019M662517]
  2. Program for Science & Technology Innovation Talents in Universities of Henan Province [19HASTIT001]

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The dysfunction of the intestinal epithelial barrier contributes to local or systemic infection and inflammation. Some lactic acid bacteria (LAB) strains had been shown to improve the conditions of barrier function and, for this reason, are recognized as probiotics.Weissella cibaria, a species belonging to the LAB group, is known to promote several health benefits. However, the role ofW. cibariain regulating the integrity of the intestinal epithelial barrier has not yet been investigated. In this study,W. cibariaMW01 was isolated from Chinese sauerkraut and was selected based on its functional features, such as gastric juice and bile salt tolerance, besides antagonistic activity against pathogenic bacteria. In a cellular model of the intestinal barrier, it was observed thatW. cibariawas able to adhere more efficiently thanLactobacillus rhamnosusGG in Caco-2 cells. Moreover, the LPS-induced inflammation in Caco-2 cells was attenuated by the treatment withW. cibariaMW01, which reduced the synthesis of TNF-alpha, IL-6, and IL-8. In addition, it was noted that the treatment withW. cibariaMW01 recovered the integrity of the Caco-2 cell monolayer exposed to LPS. Furthermore,W. cibariaMW01 significantly alleviated LPS-induced downregulation of tight junction proteins (TJP) (claudin, occludin, and tight junction protein-1). Mechanistically,W. cibariaMW01 inhibited the translocation of NF-kappa B to the nucleus and deactivated the MLCK-pMLC pathway during LPS exposure. Thus,W. cibariaMW01, as a potential probiotic, can protect intestinal epithelial barrier function by regulating inflammation and expression of TJP via the NF-kappa B-mediated MLCK-pMLC pathway.

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