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Abstract
In recent decades, research on coinfections involving influenza A and Streptococcus pneumoniae has intensified due to the heightened mortality associated with such cases. While influenza B is prevalent during seasonal outbreaks, limited exploration has been undertaken to understand if coinfection with S. pneumoniae contributes to increased disease severity. Recent case studies highlight the association between influenza B and bacterial coinfection, emphasizing a heightened risk of severe disease, particularly due to bacterial-associated pneumonia. Despite studies on influenza A coinfection, a gap exists in understanding the immune response to influenza B coinfection. A more comprehensive exploration of immune responses in influenza B and S. pneumoniae coinfections could pave the way for improved clinical treatment strategies.Influenza viruses, known for producing neuraminidase, disrupt the respiratory tract's protective mucins, facilitating bacterial colonization. Coinfection with influenza A has been linked to increased S. pneumoniae colonization in the upper respiratory tracts, progressing to the lower respiratory tract. This phenomenon is attributed to influenza viruses exposing sialic acids, facilitating invasive S. pneumoniae strain colonization.
Coinfection with S. pneumoniae and influenza A has been shown to modify the respiratory microbiome and metabolome. The heightened S. pneumoniae colonization leads to a shift in the abundance of bacteria within the natural microbiota. Additionally, alterations in energy demands and metabolic changes attributed to increased immune response are observed.
While previous research focuses on influenza A and S. pneumoniae coinfections, this study anticipates similar responses in influenza B coinfection. Utilizing the C57BL/6 mouse model, pro-inflammatory responses following secondary bacterial infection led to elevated bacterial burdens and decreased pulmonary clearance, ultimately resulting in heightened mortality. These responses include increased cytokines, chemokines, neutrophil infiltration, and decreased alveolar macrophage recruitment. The intricate interplay between alterations in the microbiome, immune responses, and the metabolome during coinfection sheds light on host responses' complexity. This emphasizes the profound impact of microbial interactions on immune and metabolic pathways.