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Lactobacillus rhamnosus JB3 inhibits Helicobacter pylori infection through multiple molecular actions
Author(s) -
Do Anh Duy,
Chang ChunChi,
Su ChiuHsian,
Hsu YuanMan
Publication year - 2021
Publication title -
helicobacter
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.206
H-Index - 79
eISSN - 1523-5378
pISSN - 1083-4389
DOI - 10.1111/hel.12806
Subject(s) - lactobacillus rhamnosus , helicobacter pylori , microbiology and biotechnology , antigen , biology , tlr4 , apoptosis , pathogenesis , multiplicity of infection , virulence , bacteria , immunology , lactobacillus , immune system , gene , virus , biochemistry , genetics
Background Eradication of Helicobacter pylori infection is the most direct and effective way for preventing gastric cancer. Lactic acid bacteria are considered as alternative therapeutic agents against H .  pylori infection. Methods Effects of Lactobacillus rhamnosus JB3 (LR‐JB3) on the virulence gene expression of H .  pylori and infection‐induced cellular responses of AGS cells were investigated by co‐cultivating infected AGS cells with different multiplicity of infections (MOIs) of LR‐JB3. Results LR‐JB3, specifically at a MOI of 25, suppressed the association ability of H .  pylori and its induced IL‐8 levels, as well as the mRNA levels of vacA , sabA , and fucT of H .  pylori , infection‐induced Lewis (Le) x antigen and Toll‐like receptor 4 (TLR4) expressions in AGS cells. However, the apoptosis mediated by infection was inhibited by LR‐JB3 in a dose‐dependent manner. In addition, autoinducer (AI)‐2 was observed to have increased the association ability and fucT expression of H .  pylori , and Le x antigen and TLR4 expression of AGS cells. Interestingly, an unknown bioactive cue was hypothesized to have been secreted from LR‐JB3 at a MOI of 25 to act as an antagonist of AI‐2. Conclusions LR‐JB3 possesses various means to interfere with H .  pylori pathogenesis and infection‐induced cellular responses of AGS cells to fight against infection.

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