Enterococcus faecalis FK-23 affects alveolar-capillary permeability to attenuate leukocyte influx in lung after influenza virus infection.

Infection with influenza A virus, one of the most common life-threatening viruses, causes the accumulation of inflammatory cells in the lung, which is directly correlated with influenza-associated morbidity and mortality. In this study, we investigated the potential of lysozyme-treated Enterococcus faecalis FK-23 (LFK) to prevent influenza in influenza virus-infected mice. C57BL/6N mice were orally administered LFK and intranasally infected with influenza virus A/Puerto Rico/8/34 (H1N1) at lethal doses. After infection with influenza A virus, the survival rate of the LFK-administered mice was significantly higher than that of saline-administered mice. Staining of lung sections with hematoxylin-eosin, and cell counts of lung and bronchoalveolar lavage fluid showed that oral administration of LFK suppressed the excessive infiltration of leukocytes into the lung after viral infection. Extravasation assay revealed that the arrest was mediated by modulation of pulmonary alveolar-capillary permeability. Expression levels of genes involved in matrix degradation, which are correlated with vascular permeability, were downregulated in LFK-administered mice. These findings suggest that stabilizing the integrity of the alveolar-capillary barrier by the administration of LFK improves survival rate.