Researchers from the Icahn School of Medicine at Mount Sinai (USA), together with research groups from CEU and the Carlos III Health Institute (ISCIII), have demonstrated in a preclinical mouse model that influenza vaccination not only protects against the virus itself but also modulates the immune response to reduce mortality associated with secondary bacterial infections. This study, published in the Journal of Virology, explores mechanisms that may be relevant to human health.
Secondary bacterial infections, such as those caused by Streptococcus pneumoniae, are among the leading causes of severe complications and death during annual influenza epidemics in at-risk populations. The study, whose first authors are Juan García-Bernalt Diego and Javier Arranz-Herrero, was coordinated in the United States by Michael
Schotsaert and supported by the Virology and Innate Immunity groups at CEU, led by Estanislao Nistal Villán, and by the ISCIII group directed by Jordi Ochando. This research continues the effort to understand why these co-infections exacerbate disease severity and how vaccination can mitigate that risk.
Key findings in the murine model
• A single dose of the trivalent inactivated influenza vaccine (TIV) reduced mortality in simultaneous viral and bacterial co-infections from 50% to 15%, and in superinfections (bacterial infection one week after viral infection) from 100% to 50%.
• Vaccination lowered viral and bacterial loads, controlled pulmonary inflammation, and prevented the massive loss of alveolar macrophages.
• A reduction in neutrophil infiltration and modulation of their activation was observed, together with an increase in eosinophils, suggesting a more controlled inflammatory response compared with that seen in unvaccinated animals.
• The vaccine reduced the production of pro-inflammatory cytokines and promoted a more balanced humoral response in vaccinated, co-infected animals compared with their unvaccinated counterparts.
Implications
Although this is a mouse model, the findings provide translational insights into how influenza vaccination could reduce bacterial complications in humans, reinforcing its role as a key preventive tool. “This study is further evidence of the need to understand how trained immunity works in controlling the memory of the innate immune system,” notes Jordi Ochando.
“Our aim is to understand why influenza opens the door to lethal bacterial infections and how vaccination can change this scenario,” explains Michael Schotsaert. Estanislao Nistal Villán adds that “infections caused by different pathogens can exacerbate immune responses, and influenza vaccination may help to better control the heightened immune response during influenza-associated co-infections.”