Acute infection with influenza virus enhances susceptibility to fatal pneumonia followingStreptococcus pneumoniaeinfection in mice with chronic pulmonary colonization withPseudomonas aeruginosa

Abstract

SUMMARYWe established a mouse model in which fatal pneumonia was induced by pneumococcal superinfection following influenza virus infection in chronic Pseudomonas aeruginosa infected mice. In this mouse model, influenza virus infection caused a significant increase in inflammatory cells, cytokines and severe tissue damage in the lungs of these P. aeruginosa infected mice, before pneumococcal infection. Intrapulmonary virus titres were significantly increased in mice with chronic P. aeruginosa infection, compared with control mice. Neutrophil function analysis showed significant reduction of myeloperoxidase (MPO) activity and lysozyme secretion by influenza virus infection in these mice. Our results suggest that influenza virus infection may play an important role in inducing pneumococcal pneumonia in chronic P. aeruginosa infected mice. Our results suggested that our mouse model is useful for investigating the pathogenesis of influenza virus infection in patients with chronic lung infection.

Postinfluenza Bacterial Pneumonia: Host Defenses Gone Awry

“…Despite elevated numbers of neutrophils recruited to the airways, there are defects in the function of these cells, including decreased phagocytic activity, myeloperoxidase production, respiratory burst, and lysozyme secretion (LeVine and others 2001; Seki and others 2004;McNamee and Harmsen 2006). Studies also suggest increased apoptosis and reduced survival in neutrophils coinfected with influenza virus and S. pneumoniae (Engelich and others 2001).…”

Neutrophils: Neglected Players in Viral Diseases

“…Influenza virus infections are often followed by secondary bacterial infections in the respiratory tract (Morens et al, 2008). Several studies demonstrated that neutrophils were unable to eliminate bacteria efficiently after influenza virus infection because of the inability to degranulate (Abramson et al, 1982a(Abramson et al, , 1982bDebets-Ossenkopp et al, 1982;Pang et al, 2000;Seki et al, 2004).…”

A Patient with Fulminant Influenza-Related Bacterial Pneumonia Due to Streptococcus pneumoniae Followed by Mycobacterium tuberculosis Infection

“…A case of fulminant primary influenza pneumonia that developed into secondary bacterial pneumonia has been reported (11), and an increase in bacterial pneumonia severity due to co-infection with influenza virus has been reported (12). These synergic effects might be enhanced by host factors mediated through immunological reactions, including activations of innate immunities and neutrophils, as we previously reported (13)(14)(15)(16)(17).…”