Oral administration of heat-killed Lactobacillus pentosus strain b240 augments protection against influenza virus infection in mice
Host-defense mechanisms against influenza virus (IFV) infection involve both innate and acquired immunities. Among other components, secretory immunoglobulin A (SIgA) in the airway mucosa plays a particularly pivotal role in preventing IFV infection. Among 150 strains of lactic acid bacteria, Lactob...
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Veröffentlicht in: | International immunopharmacology 2011-02, Vol.11 (2), p.199-203 |
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Zusammenfassung: | Host-defense mechanisms against influenza virus (IFV) infection involve both innate and acquired immunities. Among other components, secretory immunoglobulin A (SIgA) in the airway mucosa plays a particularly pivotal role in preventing IFV infection. Among 150 strains of lactic acid bacteria, Lactobacillus pentosus strain b240 (b240) has the highest IgA-inducing potency in mouse Peyer's patch cells. We previously reported a practical new finding that oral ingestion of nonviable heat-killed b240 elevates salivary IgA secretion in humans. The present study aimed to determine if nonviable b240 can prevent IFV infection in mice.
In a BALB/c mouse model infected with lethal levels of IFV A/PR8/34 (H1N1), oral administration of b240 for 3weeks by gavage prior to IFV infection significantly prolonged the survival period. For IFV infection at nonlethal levels, the infectious titers of IFV in the lungs 7days after infection were significantly reduced after similar b240 administration. Both anti-IFV IgA and immunoglobulin G titers in bronchoalveolar lavage fluid and plasma on day 7 were significantly higher in the b240-treated group than the control group. The augmentation of the anti-IFV immune response by b240 application was preliminarily confirmed by the elevated production of IFV-driven T-cell factors during mixed lymphocyte reactions with b240-primed splenocytes.
These results suggest that oral nonviable heat-killed b240 intake can facilitate protection against IFV infection. |
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ISSN: | 1567-5769 1878-1705 |
DOI: | 10.1016/j.intimp.2010.11.019 |