Virology. 2014 Jul 3;462-463C:254-265. doi: 10.1016/j.virol.2014.06.019. [Epub ahead of print]
Pneumolysin expression by streptococcus pneumoniae protects colonized mice from influenza virus-induced disease.
Wolf AI1, Strauman MC1, Mozdzanowska K1, Williams KL1, Osborne LC2, Shen H2, Liu Q1, Garlick D1, Artis D2, Hensley SE1, Caton AJ1, Weiser JN2, Erikson J3.
Abstract
The response to influenza virus (IAV) infection and severity of disease is highly variable in humans. We hypothesized that one factor contributing to this variability is the presence of specific respiratory tract (RT) microbes. One such microbe is Streptococcus pneumoniae (Sp) that is carried asymptomatically in the RT of many humans. In a mouse co-infection model we found that in contrast to secondary bacterial infection that exacerbates disease, Sp colonization 10 days prior to IAV protects from virus-induced morbidity and lung pathology. Using mutant Sp strains, we identified a critical role for the bacterial virulence factor pneumolysin (PLY) in mediating this protection. Colonization with the PLY-sufficient Sp strain induces expression of the immune-suppressive enzyme arginase 1 in alveolar macrophages (aMø) and correlates with attenuated recruitment and function of pulmonary inflammatory cells. Our study demonstrates a novel role for PLY in Sp-mediated protection by maintaining aMø as "gatekeepers" against virus-induced immunopathology.
Copyright © 2014. Published by Elsevier Inc.
KEYWORDS:
Alveolar macrophages; Arginase I; Immunopathology; Inflammatory monocytes; Influenza virus; Pneumolysin; Protection; Respiratory tract co-infection; Streptococcus pneumoniae; iNOS
PMID: 24999050 [PubMed - as supplied by publisher]
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