The role of GPR84 and IL-36R/IL-36γ in respiratory infections

Influenza infections are responsible for millions of deaths every year and may facilitate secondary bacterial infections that increased host immunopathology and severity of disease. Current strategies and treatments for influenza infections are limited. Influenza virus is notably a virus that undergo rapid antigenic drifts, which makes vaccines less efficient. Vaccines also have an application against bacteria; however, they only target specific strains of bacteria, which allow opportunistic infections by other strains. Additionally, bacteria are becoming more resistant to antibiotics. This has increased the necessity for new treatments and therapeutical approaches to treat these microbial infections. Targeting specific microbial pathways is difficult and costly, so this study proposes that targeting and modulating the host immune response to these pathogens would be a useful strategy to deal with these infections. GPR84 is a proinflammatory receptor upregulated by IL-36γ administration and low-grade inflammation. GPR84 is also involved in the immune response to bacterial infections, revealing this receptor as a potential target to boost the host 50 immune system against bacterial infection. IL-36 cytokines are increased during influenza infection and contribute to the tissue lung damage and to secondary bacterial infections. Thus, this pathway is also a potential target and should be investigated as a possible therapeutical approach to reduce the risk of secondary bacterial infections. These studies will increase the understanding of these mechanisms and how they may be targeted to improve inflammation during influenza infection and improve the immune system to fight against bacterial infections.