Inflammation and the Interconnections Between Influenza and Pneumococcal Disease

A new study using a mouse model suggests that an inflammatory response to influenza infection makes patients more susceptible to developing invasive pneumococcal disease.

Clinicians have known for some time that when patients stay current with both influenza and pneumococcal vaccines, they experience less morbidity and mortality from both influenza and invasive pneumococcal disease than if they had received just 1 of the vaccinations. It is unclear, however, whether this synergy is due to induction of an aberrant immune response resulting from systemic inflammation or to induced immunosuppression when viruses disturb neutrophil function.

Researchers have determined that people with an inflammation response underway are more likely to be colonized with Streptococcus pneumoniae (pneumococcus). Chronic lung inflammation also predisposes elderly people to pneumococcal pneumonia. With approximately 80% of school children colonized with pneumococcus, childhood otitis media (OM) is a particular concern during influenza outbreaks. (OM can lead to permanent hearing loss, learning disabilities, and often-fatal meningitis.)

In a study published online on January 14, 2013, in Infection and Immunity, researchers studied influenza A virus infection in a mouse model to determine why such an infection predisposes individuals to secondary pneumococcal pneumonia, sepsis, meningitis, or OM. The researchers focused on bacterial OM specifically, and implanted human middle ear epithelial cells in the mice. After infecting the mice with influenza virus and exposing them to pneumococcus, the researchers found that neutrophils were the predominant cellular infiltrate in the middle ear and that pneumococcal bacteria migrated to areas replete with middle ear neutrophils.

The researchers determined that the influenza virus created a pro-inflammatory response in the middle ear cavity. These findings, much like those that show lung inflammation invites pneumococcal pneumonia, suggest that an inflammatory response to influenza infection mediates pneumococcal replication. The study has significant limitations in terms of the application of its results to humans, including that the influenza strain employed was different from the strain that usually infects humans. Nonetheless, the study’s findings suggest that preventing viral disease, limiting viral replication, and addressing middle ear inflammation may help decrease OM in children. In addition, the results provide further support for vaccination against influenza and pneumococcal disease in vulnerable populations.

Ms. Wick is a visiting professor at the University of Connecticut School of Pharmacy and a freelance writer from Virginia.