medwireNews: Pneumococcal otitis media (OM) may develop as a result of proinflammatory responses in the middle ear cavity to influenza A virus (IAV) hemagglutinin, suggest Australian study findings.
"Our findings suggest that it is the inflammatory response to IAV infection that mediates pneumococcal replication… in the middle ear cavity, which may have important implications for the treatment of pneumococcal OM," say Kirsty Short (University of Melbourne, Victoria) and co-authors in Infection and Immunity.
Co-infection with Streptococcus pneumoniae and IAV often triggers OM, yet previous studies have been unable to clarify the role of IAV in the pathogenesis of pneumococcal-influenza virus OM.
Using a mouse model, the team observed an increased incidence of pneumococcal OM following infection with H3N2 (rather than H1N1) IAV strains in infant mice. This, according to the researchers, suggests that viral factors important in secondary bacterial disease are specific for each disease phenotype.
They found that viral hemagglutinin was important in controlling the development of secondary pneumococcal OM, through its upregulatory effect on IAV replication in the middle ear. Furthermore, viral H3N2 strains were able to efficiently replicate, and induced an inflammatory response in the middle ear, which was important for pneumococcal outgrowth.
Indeed, infection with H3N2 viral strains (HKx31, Port Chalmers/73, and Mem/71) resulted in significantly higher bacterial titers in the middle ear compared with H1N1 strains (approximately 105 vs 103 bacteria).
In addition, in vitro infection of human middle ear epithelial cells with various viral strains showed significantly higher levels of interleukin (IL)-6 and IL-8 with H3N2 relative to H1N1 strains, validating the results seen in mice.
The researchers say that the increased infection rate with H3N2 strains is consistent with observations that in human populations, bacterial OM is associated with more H3N2 infections than H1N1 infections.
"Should our mouse and in vitro models accurately mimic disease development in the human population, our data would suggest that limiting viral replication and inflammation in the middle ear may be key in preventing secondary pneumococcal OM," conclude the authors.
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