In vitro investigation of the effects of Lactobacillus delbrueckii ssp. bulgaricus OLL1073R-1 exopolysaccharides on tight junction damage caused by influenza virus infection

Author:

Ishikawa Hiroki1ORCID,Kuno Yoshihiro12,Yokoo Takehiro3,Nagashima Ryuichi14,Takaki Takashi5,Sasaki Hiraku6,Kohda Chikara1,Iyoda Masayuki12

Affiliation:

1. Department of Microbiology and Immunology, Showa University School of Medicine , Shinagawa-ku, Tokyo, 142-8555 , Japan

2. Division of Nephrology, Department of Medicine, Showa University School of Medicine , Shinagawa-ku, Tokyo, 142-8666 , Japan

3. Food Microbiology and Function Research Laboratories, R&D Division, Meiji Co., Ltd , Hachioji, Tokyo, 192-0919 , Japan

4. Division of Immunology, Department of Biosciences, Kitasato University School of Science , Sagamihara, Kanagawa, 252-0373 , Japan

5. Division of Electron Microscopy,Showa University , Shinagawa-ku, Tokyo, 142-8555 , Japan

6. Department of Health Science, Faculty of Health and Sports Science, Juntendo University , Inzai, Chiba, 270-1695 , Japan

Abstract

Abstract It is a problem that influenza virus infection increases susceptibility to secondary bacterial infection in lungs leading to lethal pneumonia. We previously reported that exopolysaccharides (EPS) derived from Lactobacillus delbrueckii ssp. bulgaricus OLL1073R-1 (OLL1073R-1) could prevent against influenza virus infection followed by secondary bacterial infection in vitro. Therefore, the present study assessed whether EPS derived OLL1073R-1 protects the alveolar epithelial barrier disfunction caused by influenza virus infection. After A549 cells treated with EPS or without EPS were infected influenza virus A/Puerto Rico/8/34 (IFV) for 12 h, the levels of tight junction genes expression and inflammatory genes expression were measured by reverse transcription polymerase chain reaction. As results, EPS treatment could protect against low-titer IFV infection, but not high-titer IFV infection, followed by suppression of the increased expression of inflammatory cytokine gene levels and recovery of the decrease in the expression level of ZO-1 gene that was caused by low-titer IFV infection, leading to an improvement trend in the barrier function. Our findings showed that EPS derived from OLL1073R-1 could inhibit low-titer IFV infection leading to maintenance of the epithelial barrier function through the suppression of inflammatory cytokine genes expression.

Funder

JSPS

Publisher

Oxford University Press (OUP)

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