tetano
Editor, Senior Moderator
Am J Physiol Lung Cell Mol Physiol. 2015 May 22:ajplung.00338.2014. doi: 10.1152/ajplung.00338.2014. [Epub ahead of print]
[h=1]Influenza-induced Type I Interferon Enhances Susceptibility to Gram-negative and Gram-positive Bacterial Pneumonia in Mice.[/h] Lee B[SUP]1[/SUP], Robinson KM[SUP]1[/SUP], McHugh KJ[SUP]1[/SUP], Scheller EV[SUP]1[/SUP], Mandalapu S[SUP]1[/SUP], Chen C[SUP]2[/SUP], Di YP[SUP]2[/SUP], Clay ME[SUP]1[/SUP], Enelow RI[SUP]3[/SUP], Dubin PJ[SUP]4[/SUP], Alcorn JF[SUP]5[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Suppression of Type 17 immunity by type I interferon (IFN) during influenza A infection has been shown to enhance susceptibility to secondary bacterial pneumonia. While this mechanism has been described in coinfection with Gram-positive bacteria, it is unclear if similar mechanisms may impair lung defense against Gram-negative infections. Furthermore, precise delineation of the duration of type I IFN-associated susceptibility to bacterial infection remains underexplored. Therefore, we investigated the effects of preceding influenza A virus infection on subsequent challenge with the Gram-negative bacteria Escherichia coli and Pseudomonas aeruginosa, and the temporal association between IFN expression with susceptibility to Staphylococcus aureus challenge in a mouse model of influenza and bacterial coinfection. Here, we demonstrate that preceding influenza A virus led to increased lung E. coli and P. aeruginosa bacterial burden, which was associated with suppression of Type 17 immunity and attenuation of antimicrobial peptide expression. Enhanced susceptibility to S. aureus coinfection ceased at day 14 of influenza infection, when influenza-associated type I IFN levels had returned to baseline levels, further suggesting a key role for type I IFN in coinfection pathogenesis. These findings further implicate type I IFN-associated suppression of Type 17 immunity and antimicrobial peptide production as a conserved mechanism for enhanced susceptibility to both Gram-positive and Gram-negative bacterial coinfection during influenza infection.
Copyright ? 2014, American Journal of Physiology - Lung Cellular and Molecular Physiology.
[h=4]KEYWORDS:[/h] Escherichia coli; Influenza A; Staphylococcus aureus; Type I interferon; coinfection
PMID: 26001778 [PubMed - as supplied by publisher]
[h=1]Influenza-induced Type I Interferon Enhances Susceptibility to Gram-negative and Gram-positive Bacterial Pneumonia in Mice.[/h] Lee B[SUP]1[/SUP], Robinson KM[SUP]1[/SUP], McHugh KJ[SUP]1[/SUP], Scheller EV[SUP]1[/SUP], Mandalapu S[SUP]1[/SUP], Chen C[SUP]2[/SUP], Di YP[SUP]2[/SUP], Clay ME[SUP]1[/SUP], Enelow RI[SUP]3[/SUP], Dubin PJ[SUP]4[/SUP], Alcorn JF[SUP]5[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Suppression of Type 17 immunity by type I interferon (IFN) during influenza A infection has been shown to enhance susceptibility to secondary bacterial pneumonia. While this mechanism has been described in coinfection with Gram-positive bacteria, it is unclear if similar mechanisms may impair lung defense against Gram-negative infections. Furthermore, precise delineation of the duration of type I IFN-associated susceptibility to bacterial infection remains underexplored. Therefore, we investigated the effects of preceding influenza A virus infection on subsequent challenge with the Gram-negative bacteria Escherichia coli and Pseudomonas aeruginosa, and the temporal association between IFN expression with susceptibility to Staphylococcus aureus challenge in a mouse model of influenza and bacterial coinfection. Here, we demonstrate that preceding influenza A virus led to increased lung E. coli and P. aeruginosa bacterial burden, which was associated with suppression of Type 17 immunity and attenuation of antimicrobial peptide expression. Enhanced susceptibility to S. aureus coinfection ceased at day 14 of influenza infection, when influenza-associated type I IFN levels had returned to baseline levels, further suggesting a key role for type I IFN in coinfection pathogenesis. These findings further implicate type I IFN-associated suppression of Type 17 immunity and antimicrobial peptide production as a conserved mechanism for enhanced susceptibility to both Gram-positive and Gram-negative bacterial coinfection during influenza infection.
Copyright ? 2014, American Journal of Physiology - Lung Cellular and Molecular Physiology.
[h=4]KEYWORDS:[/h] Escherichia coli; Influenza A; Staphylococcus aureus; Type I interferon; coinfection
PMID: 26001778 [PubMed - as supplied by publisher]