@article{mbs:/content/journal/jmm/10.1099/jmm.0.009662-0, author = "Fang, Hsu-Wei and Fang, Shiuh-Bin and Chiang Chiau, Jen-Shiu and Yeung, Chun-Yan and Chan, Wai-Tao and Jiang, Chuen-Bin and Cheng, Mei-Lien and Lee, Hung-Chang", title = "Inhibitory effects of Lactobacillus casei subsp. rhamnosus on Salmonella lipopolysaccharide-induced inflammation and epithelial barrier dysfunction in a co-culture model using Caco-2/peripheral blood mononuclear cells", journal= "Journal of Medical Microbiology", year = "2010", volume = "59", number = "5", pages = "573-579", doi = "https://doi.org/10.1099/jmm.0.009662-0", url = "https://www.microbiologyresearch.org/content/journal/jmm/10.1099/jmm.0.009662-0", publisher = "Microbiology Society", issn = "1473-5644", type = "Journal Article", keywords = "MCP-1, monocyte chemoattractant protein 1", keywords = "IL-8, interleukin-8", keywords = "NF-κB, nuclear factor-kappa B", keywords = "TEER, transepithelial electrical resistance", keywords = "TNF-α, tumour necrosis factor alpha", keywords = "IEC, intestinal epithelial cell", keywords = "TGF-β1, transforming growth factor-β1", keywords = "PBMC, peripheral blood mononuclear cell", abstract = "In this study, we investigated the anti-inflammatory and reinforcing barrier effects of Lactobacillus casei subsp. rhamnosus (Lcr35) on Caco-2 intestinal epithelial cells already exposed to Salmonella LPS. Using the Transwell co-culture model, Salmonella LPS was apically added to polarized Caco-2 cells co-cultured with peripheral blood mononuclear cells (PBMCs) in the basolateral compartment. LPS-stimulated Caco-2 cells were incubated with Lcr35 for 1, 6, 24 or 48 h. Apical inoculation of Lcr35 after 48 h significantly inhibited the basolateral secretion of interleukin-8 (IL-8) in the Caco-2/PBMC co-culture. The PCR analysis showed that Lcr35 significantly downregulated mRNA expression of monocyte chemoattractant protein 1 (MCP-1) (P<0.05) and had a trend of decreasing mRNA expression of IL-8 (P=0.05), but did not alter mRNA expression of transforming growth factor-β1 in LPS-stimulated Caco-2 cells at 48 h after addition of Lcr35. Compared to non-LPS-pretreated controls, transepithelial electrical resistance (TEER) of the polarized Caco-2 cell monolayers pretreated with LPS for 48 h was decreased by 9.9 % (P<0.05). Additionally, compared to those cells only treated with LPS, apical co-incubation with Lcr35 showed biphasic TEER levels increased by 12.1 % (P<0.001), 5.7 % (P<0.05) and 86.8 % (P<0.001) in the Caco-2 cell monolayers compared to those without Lcr35 treatment after 1, 6 and 48 h, respectively. In conclusion, Lcr35 can exert anti-inflammatory effects and ameliorate barrier dysfunction in the Salmonella LPS-pretreated inflamed intestinal epithelium in vitro.", }