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Effects of influenza infection on neutrophil function and increased susceptibility to a secondary Streptococcus pneumoniae infection
Author(s) -
McNamee Lynnelle,
Harmsen Allen
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.4.a213-d
Subject(s) - phagocytosis , streptococcus pneumoniae , immunology , bone marrow , opsonin , microbiology and biotechnology , flow cytometry , neutrophile , influenza a virus , granulocyte , nasal administration , medicine , biology , inflammation , virus , antibiotics
The purpose of this study was to determine whether an influenza infection affects neutrophil function, thereby increasing susceptibility to a secondary Streptococcus pneumoniae infection. To determine this, we measured the phagocytosis and reactive oxygen species (ROS) generation by neutrophils in the lungs and bone marrow of uninfected and influenza‐infected mice. Mice were infected intranasally with 600 PFUs of PR8 influenza virus in 100 μL HBSS for 3 or 6 days. Control mice received 100 μL HBSS intranasally. To elicit a neutrophil response in the lungs of uninfected mice, mice were exposed to aerosolized LPS (10 mg/mL) for 20 minutes, and the neutrophil response was allowed to develop for 8 hours before the neutrophils were collected. Neutrophils were collected from the lungs and bone marrow from all groups of mice. S. pneumoniae was labeled with DiI and opsonized with fresh mouse serum. To measure phagocytosis, neutrophils were incubated with the labeled S. pneumoniae . To measure ROS, di(acetoxymethyl ester) was added to the leukocytes. Phagocytosis and ROS were measured using flow cytometry at incubation times of 0 and 60 minutes. We found that a prior influenza infection reduced the phagocytosis and ROS capabilities in the lungs, and to a lesser extent the bone marrow, compared to uninfected or LPS‐challenged mice. In conclusion, a prior influenza infection appears to increase susceptibility to a secondary S. pneumoniae infection by reducing neutrophil function.