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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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Related in: MedlinePlus

L. fructosus C2 decreased pathogenic bacteria induced increases in macromolecular permeability (A) and TER (B). Polarized monolayers were treated with L. fructosus C2 (MOI 200:1) or pathogens (ETEC or S. typhimurium, MOI 20:1) either alone or simultaneously for 2 h. Integrated intensities of dextran diffused into the basolateral compartments were detected 2 h after dextran addition to the apical compartment. TER values were detected at 0, 1, 2, 3, 4, 6, and 12 h post co-infection. *P < 0.05, as determined by ANOVA. The data represent results from four independent experiments.
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Figure 1: L. fructosus C2 decreased pathogenic bacteria induced increases in macromolecular permeability (A) and TER (B). Polarized monolayers were treated with L. fructosus C2 (MOI 200:1) or pathogens (ETEC or S. typhimurium, MOI 20:1) either alone or simultaneously for 2 h. Integrated intensities of dextran diffused into the basolateral compartments were detected 2 h after dextran addition to the apical compartment. TER values were detected at 0, 1, 2, 3, 4, 6, and 12 h post co-infection. *P < 0.05, as determined by ANOVA. The data represent results from four independent experiments.

Mentions: The results demonstrated that treatment with L. fructosus C2 alone did not alter the diffusion of the FD70s from apical to basolateral Millicell compartments [relative integrated intensity (RI) compared to untreated monolayers] (Figure 1A). However, compared to the control group, ETEC K88 or S. typhimurium SL1344 infection did exhibit a remarkable increase in the permeability to the dextran probe (P < 0.05). Treatment of Caco-2 cells with L. fructosus C2 and pathogens (ETEC K88 or S. typhimurium SL1344) simultaneously, the permeability to the dextran probe was decreased significantly (P < 0.05). These results revealed that L. fructosus C2 preserved intestinal epithelial cell integrity.


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 decreased pathogenic bacteria induced increases in macromolecular permeability (A) and TER (B). Polarized monolayers were treated with L. fructosus C2 (MOI 200:1) or pathogens (ETEC or S. typhimurium, MOI 20:1) either alone or simultaneously for 2 h. Integrated intensities of dextran diffused into the basolateral compartments were detected 2 h after dextran addition to the apical compartment. TER values were detected at 0, 1, 2, 3, 4, 6, and 12 h post co-infection. *P < 0.05, as determined by ANOVA. The data represent results from four independent experiments.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 1: L. fructosus C2 decreased pathogenic bacteria induced increases in macromolecular permeability (A) and TER (B). Polarized monolayers were treated with L. fructosus C2 (MOI 200:1) or pathogens (ETEC or S. typhimurium, MOI 20:1) either alone or simultaneously for 2 h. Integrated intensities of dextran diffused into the basolateral compartments were detected 2 h after dextran addition to the apical compartment. TER values were detected at 0, 1, 2, 3, 4, 6, and 12 h post co-infection. *P < 0.05, as determined by ANOVA. The data represent results from four independent experiments.
Mentions: The results demonstrated that treatment with L. fructosus C2 alone did not alter the diffusion of the FD70s from apical to basolateral Millicell compartments [relative integrated intensity (RI) compared to untreated monolayers] (Figure 1A). However, compared to the control group, ETEC K88 or S. typhimurium SL1344 infection did exhibit a remarkable increase in the permeability to the dextran probe (P < 0.05). Treatment of Caco-2 cells with L. fructosus C2 and pathogens (ETEC K88 or S. typhimurium SL1344) simultaneously, the permeability to the dextran probe was decreased significantly (P < 0.05). These results revealed that L. fructosus C2 preserved intestinal epithelial cell integrity.

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