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As spring emerges from the shadows of a cold, dark winter, we are again left to reflect on the ravages of another influenza season. Based on the emergent data from Australia,1 the 2017–2018 outbreak in the Northern Hemisphere was predicted to be particularly severe and so it proved to be. Disease severity can be driven by a number of factors, including shifts in the viral genome, but host innate immune responses also play a role, most notably in the lethal cytokine storm response to avian influenza strains.2
Macrophages are the predominant innate immune cell in the human airway and critical for an appropriate protective response to bacterial, fungal and viral infections. These cells enhance viral clearance, being essential for both viral antigen presentation to mucosal T cells3 and the development of neutralising antibodies.4 Furthermore, when macrophages are depleted, there is increased lung pathology5 in response to viral infection demonstrating the central role of macrophages in ensuring that virus control does not compromise host survival. In the majority of cases, such mechanisms ensure that lung inflammation is kept to a minimum so that pneumonias do not develop. However, it is known that influenza infection can lead to both primary and secondary bacterial pneumonias,6 although whether as a result of virus or host factors is unclear. Pneumonias are primarily associated with massive neutrophil influx into the lung leading to compromised gas exchange but there are conflicting reports as to whether the role of the neutrophil in viral infections is protective or pathological.7 The study by Peiró et al8 has provided further insight into the complex interplay between macrophages and neutrophils in a mouse model of influenza infection.
Peiró and colleagues first demonstrated that the pleiotropic proinflammatory cytokine, interleukin 1-beta (IL-1β), is induced by influenza …
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