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Lactobacillus protects the integrity of intestinal epithelial barrier damaged by pathogenic bacteria.

Yu Q, Yuan L, Deng J, Yang Q - Front Cell Infect Microbiol (2015)

Bottom Line: Moreover, some Lactobacillus could inhibit the adhesion of the pathogens and protect the integrity of the cell junction and mucosal barrier.This research focused on the potential therapeutic effect of Lactobacillus fructosus (L. fructosus) C2 to attenuate ETEC K88 or S. typhimurium SL1344 induced changes to mucosal barrier.The results demonstrated that treatment of polarized Caco-2 cells with L. fructosus C2 reduced the permeation of dextran, and expression of IL-8, p-ERK, and p-JNK when cells were infected with pathogenic bacteria.

View Article: PubMed Central - PubMed

Affiliation: College of Veterinary Medicine, Nanjing Agricultural University Nanjing, China.

ABSTRACT
Pathogens invade intestinal mucosal barrier through phagocytosis of antigen presenting cells (dendritic cell, microfold cells), or through the invasion into the intestinal epithelial directly. Some pathogens could damage the cell junction between epithelial cells and use the paracellular pathway as an entrance to invade. Moreover, some Lactobacillus could inhibit the adhesion of the pathogens and protect the integrity of the cell junction and mucosal barrier. This research focused on the potential therapeutic effect of Lactobacillus fructosus (L. fructosus) C2 to attenuate ETEC K88 or S. typhimurium SL1344 induced changes to mucosal barrier. The results demonstrated that treatment of polarized Caco-2 cells with L. fructosus C2 reduced the permeation of dextran, and expression of IL-8, p-ERK, and p-JNK when cells were infected with pathogenic bacteria. The findings indicated that L. fructosus C2 exerted a protective effect against the damage to the integrity of Caco-2 cells by ETEC or S. typhimurium infection.

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L. fructosus C2 inhibited the phosphorylation of ERK (A) and JNK (B) caused by ETEC or S. typhimurium on Caco-2 cells. Caco-2 cells were untreated (Control), infected with ETEC or S. typhimurium (MOI 20:1) alone or co-cultured with L. fructosus C2 (MOI 200:1) simultaneously for 2 h. The figure showed a western blot of immunoprecipitated ERK and JNK level, representative of four independent assays, and the densitometric values of phosphorylation of ERK and JNK normalized to total ERK and JNK. Values are means ± SE. *P < 0.05, as determined by ANOVA.
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Figure 4: L. fructosus C2 inhibited the phosphorylation of ERK (A) and JNK (B) caused by ETEC or S. typhimurium on Caco-2 cells. Caco-2 cells were untreated (Control), infected with ETEC or S. typhimurium (MOI 20:1) alone or co-cultured with L. fructosus C2 (MOI 200:1) simultaneously for 2 h. The figure showed a western blot of immunoprecipitated ERK and JNK level, representative of four independent assays, and the densitometric values of phosphorylation of ERK and JNK normalized to total ERK and JNK. Values are means ± SE. *P < 0.05, as determined by ANOVA.

Mentions: We next investigated the activation of ERK and JNK in Caco-2 cells treated with L. fructosus C2 alone or with pathogens (ETEC or S. typhimurium) simultaneously. The results demonstrated that the phosphorylation level of ERK and JNK were increased significantly while infected with ETEC K88 alone (P < 0.05) (Figure 4). However, the phosphorylation level of ERK and JNK were reduced significantly co-cultured with L. fructosus C2 and pathogens simultaneously, compared to the pathogens infected alone.


Lactobacillus protects the integrity of intestinal epithelial barrier damaged by pathogenic bacteria.

Yu Q, Yuan L, Deng J, Yang Q - Front Cell Infect Microbiol (2015)

L. fructosus C2 inhibited the phosphorylation of ERK (A) and JNK (B) caused by ETEC or S. typhimurium on Caco-2 cells. Caco-2 cells were untreated (Control), infected with ETEC or S. typhimurium (MOI 20:1) alone or co-cultured with L. fructosus C2 (MOI 200:1) simultaneously for 2 h. The figure showed a western blot of immunoprecipitated ERK and JNK level, representative of four independent assays, and the densitometric values of phosphorylation of ERK and JNK normalized to total ERK and JNK. Values are means ± SE. *P < 0.05, as determined by ANOVA.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4373387&req=5

Figure 4: L. fructosus C2 inhibited the phosphorylation of ERK (A) and JNK (B) caused by ETEC or S. typhimurium on Caco-2 cells. Caco-2 cells were untreated (Control), infected with ETEC or S. typhimurium (MOI 20:1) alone or co-cultured with L. fructosus C2 (MOI 200:1) simultaneously for 2 h. The figure showed a western blot of immunoprecipitated ERK and JNK level, representative of four independent assays, and the densitometric values of phosphorylation of ERK and JNK normalized to total ERK and JNK. Values are means ± SE. *P < 0.05, as determined by ANOVA.
Mentions: We next investigated the activation of ERK and JNK in Caco-2 cells treated with L. fructosus C2 alone or with pathogens (ETEC or S. typhimurium) simultaneously. The results demonstrated that the phosphorylation level of ERK and JNK were increased significantly while infected with ETEC K88 alone (P < 0.05) (Figure 4). However, the phosphorylation level of ERK and JNK were reduced significantly co-cultured with L. fructosus C2 and pathogens simultaneously, compared to the pathogens infected alone.

Bottom Line: Moreover, some Lactobacillus could inhibit the adhesion of the pathogens and protect the integrity of the cell junction and mucosal barrier.This research focused on the potential therapeutic effect of Lactobacillus fructosus (L. fructosus) C2 to attenuate ETEC K88 or S. typhimurium SL1344 induced changes to mucosal barrier.The results demonstrated that treatment of polarized Caco-2 cells with L. fructosus C2 reduced the permeation of dextran, and expression of IL-8, p-ERK, and p-JNK when cells were infected with pathogenic bacteria.

View Article: PubMed Central - PubMed

Affiliation: College of Veterinary Medicine, Nanjing Agricultural University Nanjing, China.

ABSTRACT
Pathogens invade intestinal mucosal barrier through phagocytosis of antigen presenting cells (dendritic cell, microfold cells), or through the invasion into the intestinal epithelial directly. Some pathogens could damage the cell junction between epithelial cells and use the paracellular pathway as an entrance to invade. Moreover, some Lactobacillus could inhibit the adhesion of the pathogens and protect the integrity of the cell junction and mucosal barrier. This research focused on the potential therapeutic effect of Lactobacillus fructosus (L. fructosus) C2 to attenuate ETEC K88 or S. typhimurium SL1344 induced changes to mucosal barrier. The results demonstrated that treatment of polarized Caco-2 cells with L. fructosus C2 reduced the permeation of dextran, and expression of IL-8, p-ERK, and p-JNK when cells were infected with pathogenic bacteria. The findings indicated that L. fructosus C2 exerted a protective effect against the damage to the integrity of Caco-2 cells by ETEC or S. typhimurium infection.

Show MeSH
Related in: MedlinePlus