Influenza-induced type I interferon enhances susceptibility to gram-negative and gram-positive bacterial pneumonia in mice
| Autor: | Kevin J. McHugh, Chen Chen, Benjamin Lee, Keven M. Robinson, Michelle E. Clay, John F. Alcorn, Richard I. Enelow, Sivanarayana Mandalapu, Patricia J. Dubin, Erich V. Scheller, Y. Peter Di |
|---|---|
| Rok vydání: | 2015 |
| Předmět: |
Male
Pulmonary and Respiratory Medicine Staphylococcus aureus Physiology Receptor Interferon alpha-beta Biology medicine.disease_cause Staphylococcal infections Microbiology Mice Orthomyxoviridae Infections Interferon Immunity Physiology (medical) Escherichia coli Pneumonia Bacterial medicine Influenza A virus Animals Antimicrobial peptide production Escherichia coli Infections Mice Knockout Coinfection Pseudomonas aeruginosa Bacterial pneumonia Articles Pneumonia Cell Biology Staphylococcal Infections medicine.disease Virology Mice Inbred C57BL Disease Susceptibility Antimicrobial Cationic Peptides medicine.drug |
| Zdroj: | American Journal of Physiology-Lung Cellular and Molecular Physiology. 309:L158-L167 |
| ISSN: | 1522-1504 1040-0605 |
| DOI: | 10.1152/ajplung.00338.2014 |
| Popis: | Suppression of type 17 immunity by type I interferon (IFN) during influenza A infection has been shown to enhance susceptibility to secondary bacterial pneumonia. Although this mechanism has been described in coinfection with gram-positive bacteria, it is unclear whether 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 or 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. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|