CERELA   05438
CENTRO DE REFERENCIA PARA LACTOBACILOS
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
Role of interferons and interleukin-10 in the protection of infant mice against toll-like receptor 3-mediated lung inflammatory damage and secondary pneumococcal infection induced by non-viable immunobiotic bacteria
Autor/es:
PATRICIA CLUA; ASUKA TADA; SUSANA ALVAREZ; HORTENSIA ZELAYA; HARUKI KITAZAWA; GABRIELA MARRANZINO; SUSANA SALVA; JULIO VILLENA
Lugar:
San Miguel de Tucumán
Reunión:
Simposio; V Simposio Internacional de Bacterias Lácticas (SIBAL); 2016
Institución organizadora:
CERELA-CONICET
Resumen:
Previously, we demonstrated that nasally administered non-viable Lactobacillus rhamnosus CRL1505 (HkLr05) beneficially modulates respiratory TLR3-mediated inflammation and improve the outcome of secondary pneumococcal infection of infant mice. In this work, we investigated the role of IFN-β, IFN-γ, and IL-10 in the protective activity of non-viable immunobiotic bacteria. HkLr05 was nasally administered to infant mice for 2 days and then, mice received three doses of poly(I:C) with 24 hours rest period between each administration to induce lung inflammation. Pneumococcal infection was performed at day 5 after the last poly(I:C) administration. Mice with no HkLr05 treatment were used as controls. Different groups of mice treated with HkLr05 and poly(I:C) in the same way, received an intraperitoneal injection of anti-IFN-β, anti-IFN-γ, or anti-IL-10 receptor blocking antibodies on days 2 and 4 after the last poly(I:C) administration and challenged with pneumococci on day 5. Resistance to the infection, lung tissue damage, and respiratory cytokines were evaluated. As described previously poly(I:C) administration induced a marked inflammatory-mediated impairment of lung function, and significantly increased the susceptibility of infant mice to secondary pneumococcal infection. Treatment of infant mice with HkLr05 reduced lung injuries, improved the production of IFN-β, IFN-γ, and IL-10 and decreased the susceptibility to pneumococci by reducing lung bacterial cell counts and avoiding dissemination of the pathogen into the blood. Blocking with anti-IFN-β and anti-IFN-γ antibodies significantly abolished the capacity of HkLr05 to avoid bacteremia and reduce lung bacterial cell counts, respectively (p