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2007 ; 75
(6
): 3102-11
Nephropedia Template TP
gab.com Text
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English Wikipedia
Filamentous influenza A virus infection predisposes mice to fatal septicemia
following superinfection with Streptococcus pneumoniae serotype 3
#MMPMID17403870
Speshock JL
; Doyon-Reale N
; Rabah R
; Neely MN
; Roberts PC
Infect Immun
2007[Jun]; 75
(6
): 3102-11
PMID17403870
show ga
Previous studies have demonstrated that animals exposed to Streptococcus
pneumoniae while recovering from influenza A virus infection exhibit exacerbated
disease symptoms. However, many of the current animal models exploring dual viral
and bacterial synergistic exacerbations of respiratory disease have utilized
mouse-adapted influenza virus and strains of Streptococcus pneumoniae that in
themselves are highly lethal to mice. Here we describe a mouse model of bacterial
superinfection in which a mild, self-limiting influenza virus infection is
followed by mild, self-limiting superinfection with S. pneumoniae serotype 3. S.
pneumoniae superinfection results in rapid dissemination of the bacterium from
the respiratory tract and systemic spread to all major organs of the mice,
resulting in fatal septicemia. This phenomenon in mice was observed in
superinfected animals undergoing an active viral infection as well as in mice
that had completely cleared the virus 7 to 8 days prior to superinfection.
Neutrophils were the predominant cellular inflammatory infiltrate in the lungs of
superinfected mice compared to singly infected animals. Among other cytokines and
chemokines, the neutrophil activator granulocyte colony-stimulating factor
(G-CSF) was found to be significantly overexpressed in the spleens, lungs, and
brains of superinfected animals. High G-CSF protein levels were observed in sera
and lung lavage fluid from superinfected animals, suggesting that G-CSF is a
major contributor to synergistic exacerbation of disease leading to fatal
septicemia.