title: Anti-influenza virus effects of both live and non-live Lactobacillus acidophilus L-92 accompanied by the activation of innate immunity.
abstract: The antiviral effects of both a live and non-live Lactobacillus acidophilus strain L-92 (L-92) were investigated by oral administration (10 mg/mouse per d) daily for 21 d in a mouse model infected intranasally with influenza virus (H1N1). Virus titres in the lung of mice administered either live or non-live L-92 cells daily for 15 d were repressed 6 d after virus infection compared with the control group. Natural killer (NK) activity in the orally administered non-live L-92 group was higher compared with that of the control group before virus infection and on day 6. In contrast, NK activity in the live L-92 group compared with the control group was not significantly changed on both days, but was significantly higher on day 1. In contrast, live L-92 showed a greater repression of virus proliferation compared with non-live L-92, 6 d after the infection. Live L-92 decreased the number of neutrophils in the lung and suppressed lung weight, leading to the consequent deterioration of consolidation scores of the lung. These results indicated that pretreatment of live or non-live L-92 cells had protective effects against influenza virus infection. Among the measured cytokines and chemokines, eotaxin, macrophage colony-stimulating factor, IL-1b, RANTES (regulated on activation, normal T cell expressed and secreted) and interferon-a were significantly increased in the lung: IL-17 was significantly increased in Peyer’s patch of the live L-92 group compared with the control group. A mechanistic study suggested that the enhancement of NK activity in the lung caused by stimulating various antiviral cytokines and chemokines after the oral administration of L-92 cells might be important in protecting against virus infection.
authors.affiliation: Microbiology and Fermentation Laboratory, Calpis Company Limited, 11-10, 5-Chome, Fuchinobe, Sagamihara-shi, Chuo-ku, Kanagawa 252-0206, Japan.
authors.forename: Hiroaki
authors.initials: H
authors.lastname: Goto
authors.forename: Atsuhiro
authors.initials: A
authors.lastname: Sagitani
authors.forename: Nobuhisa
authors.initials: N
authors.lastname: Ashida
authors.forename: Shinji
authors.initials: S
authors.lastname: Kato
authors.forename: Tatsuhiko
authors.initials: T
authors.lastname: Hirota
authors.forename: Tadashi
authors.initials: T
authors.lastname: Shinoda
authors.forename: Naoyuki
authors.initials: N
authors.lastname: Yamamoto
mesh_terms: D000818:Animals; D000998:Antiviral Agents / Q000627:therapeutic use*; D018925:Chemokines / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism; D004195:Disease Models, Animal; D005260:Female; D007113:Immunity, Innate; D053118:Influenza A Virus, H1N1 Subtype; D007694:Killer Cells, Natural / Q000378:metabolism; D007779:Lactobacillus acidophilus / Q000276:immunology*; D008168:Lung / Q000276:immunology* / Q000378:metabolism; D051379:Mice; D008807:Mice, Inbred BALB C; D009504:Neutrophils / Q000378:metabolism; D009929:Organ Size; D009976:Orthomyxoviridae Infections / Q000188:drug therapy* / Q000276:immunology / Q000821:virology; D010581:Peyer's Patches / Q000276:immunology / Q000378:metabolism; D019936:Probiotics / Q000627:therapeutic use*
chemical_list: D000998:Antiviral Agents; D018925:Chemokines; D016207:Cytokines