The Role of Innate Leukocytes during Influenza Virus Infection

Figure 1

Schematic representation of neutrophil-mediated host defense mechanisms during influenza virus infection. Influenza A virus- (IAV)-infected airway epithelium releases neutrophil chemoattractants: CXCL1 and CXCL2. Neutrophils traffic into infected lungs by digesting endothelial basement membrane collagen. During trafficking, they release CXCL12-loaded vesicles/membranes which provide signals for CD8⁺ T cell migration and effector function. Once in the lungs, neutrophils secrete antimicrobial peptides and cytokines, including IFNγ, to inhibit IAV replication. TNFα produced by infected airway epithelium triggers the formation of neutrophil extracellular traps (NETs) which neutralize IAV particles. Enhanced NETosis damages airway epithelium and endothelium leading to severe pneumonia.