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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 ETEC K88 or S. typhimurium SL1344 induced tight junction changes of Caco-2 cells. 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. (A,G) cells without treatment. (B,H) Cells treated with ETEC K88. (C,I) Cells treated with S. typhimurium SL1344. (D,J) Cells treated with L. fructosus C2. (E,K) Cells treated with L. fructosus C2 and ETEC K88 simultaneously. (F,L) Cells treated with L. fructosus C2 and S. typhimurium SL1344 simultaneously. Arrow showed the tight junction.
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Figure 3: L. fructosus C2 inhibited ETEC K88 or S. typhimurium SL1344 induced tight junction changes of Caco-2 cells. 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. (A,G) cells without treatment. (B,H) Cells treated with ETEC K88. (C,I) Cells treated with S. typhimurium SL1344. (D,J) Cells treated with L. fructosus C2. (E,K) Cells treated with L. fructosus C2 and ETEC K88 simultaneously. (F,L) Cells treated with L. fructosus C2 and S. typhimurium SL1344 simultaneously. Arrow showed the tight junction.

Mentions: Transmission electron microscopy of untreated Caco-2 epithelial cells revealed the tight junctions located at the apical side of cell monolayers, appear as sites where the intercellular space between neighboring cells is obliterated and the adjoining membranes appear to fuse (Figure 3A). Adherens junction and desmosomes were also visible below the tight junction. In contrast, in Caco-2 cells infected with ETEC K88 or S. typhimurium SL1344, the tight junction became wider (Figures 3B,C). When treated with L. fructosus C2 alone, Caco-2 cells presented a normal brush border and without distinct ultrastructural changes in tight junctions morphology (Figure 3D). Cells treated with L. fructosus C2 and ETEC K88 or S. typhimurium SL1344 simultaneously showed membrane disruption to a lesser extent compared with the infected group (Figures 3E,F).


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 ETEC K88 or S. typhimurium SL1344 induced tight junction changes of Caco-2 cells. 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. (A,G) cells without treatment. (B,H) Cells treated with ETEC K88. (C,I) Cells treated with S. typhimurium SL1344. (D,J) Cells treated with L. fructosus C2. (E,K) Cells treated with L. fructosus C2 and ETEC K88 simultaneously. (F,L) Cells treated with L. fructosus C2 and S. typhimurium SL1344 simultaneously. Arrow showed the tight junction.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 3: L. fructosus C2 inhibited ETEC K88 or S. typhimurium SL1344 induced tight junction changes of Caco-2 cells. 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. (A,G) cells without treatment. (B,H) Cells treated with ETEC K88. (C,I) Cells treated with S. typhimurium SL1344. (D,J) Cells treated with L. fructosus C2. (E,K) Cells treated with L. fructosus C2 and ETEC K88 simultaneously. (F,L) Cells treated with L. fructosus C2 and S. typhimurium SL1344 simultaneously. Arrow showed the tight junction.
Mentions: Transmission electron microscopy of untreated Caco-2 epithelial cells revealed the tight junctions located at the apical side of cell monolayers, appear as sites where the intercellular space between neighboring cells is obliterated and the adjoining membranes appear to fuse (Figure 3A). Adherens junction and desmosomes were also visible below the tight junction. In contrast, in Caco-2 cells infected with ETEC K88 or S. typhimurium SL1344, the tight junction became wider (Figures 3B,C). When treated with L. fructosus C2 alone, Caco-2 cells presented a normal brush border and without distinct ultrastructural changes in tight junctions morphology (Figure 3D). Cells treated with L. fructosus C2 and ETEC K88 or S. typhimurium SL1344 simultaneously showed membrane disruption to a lesser extent compared with the infected group (Figures 3E,F).

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