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

Abstract

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 of W. cibaria in regulating the integrity of the intestinal epithelial barrier has not yet been investigated. In this study, W. cibaria MW01 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 that W. cibaria was able to adhere more efficiently than Lactobacillus rhamnosus GG in Caco-2 cells. Moreover, the LPS-induced inflammation in Caco-2 cells was attenuated by the treatment with W. cibaria MW01, which reduced the synthesis of TNF-α, IL-6, and IL-8. In addition, it was noted that the treatment with W. cibaria MW01 recovered the integrity of the Caco-2 cell monolayer exposed to LPS. Furthermore, W. cibaria MW01 significantly alleviated LPS-induced downregulation of tight junction proteins (TJP) (claudin, occludin, and tight junction protein-1). Mechanistically, W. cibaria MW01 inhibited the translocation of NF-κB to the nucleus and deactivated the MLCK-pMLC pathway during LPS exposure. Thus, W. cibaria MW01, as a potential probiotic, can protect intestinal epithelial barrier function by regulating inflammation and expression of TJP via the NF-κB-mediated MLCK-pMLC pathway.

Oral nanozyme-engineered probiotics for the treatment of ulcerative colitis

“…1,4,5 Although the precise pathogenesis of UC remains controversial, a considerable number of recent studies have shown that the unavoidable pathogenic factors contributing to ulcerative colitis include both the dysfunction of the intestinal epithelial barrier and the excessive release of inflammation and oxidative stress. 6,7 Impairment of the gut barrier contributes to gut leakage, which facilitates the access of lumen stimulators, including bacteria, toxins, and antigens, to the internal organs, resulting in the occurrence and progression of chronic inflammation and abnormal immune responses. 8,9 Thus, exploring a therapeutic or prophylactic approach to restore and maintain the homeostasis of the intestinal barrier may help ameliorate the manifestations of UC.…”

Therapeutic material basis and underling mechanisms of Shaoyao Decoction-exerted alleviation effects of colitis based on GPX4-regulated ferroptosis in epithelial cells

“…Epithelial barrier loss dysfunction model in vitro was established using Caco-2 cells (1 × 106) monolayer incubated LPS (0.5 ng/mL) for 3 days [ 26 ]. Caco-2 monolayers were treated with LPS or Shaoyao Decoction medicated serum.…”

Allicin Improves Intestinal Epithelial Barrier Function and Prevents LPS-Induced Barrier Damages of Intestinal Epithelial Cell Monolayers

“…Deoxynivalenol (DON), a secondary metabolite from the fungi in the corns, could easily damage the intestinal barrier (16,17). The human colon cancer cell line Caco-2 grown in the transwell plates was commonly used as an intestinal barrier model to mimic the gut barrier of humans (18)(19)(20). However, this Caco-2 cell monolayer mimicked gut barrier has been questioned due to its characters of rapid growth and malignant proliferation.…”