Macrophages and neutrophils: dynamic duo or partners in crime?

Abstract

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 Australia1, the 2017-18 outbreak in the Northern Hemisphere was predicted to be particularly severe an 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 strains2.
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 antibodies4. 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 pneumonias6, 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 pathologic7.

More information

Identifiers

ORCID for Karl J. Staples: orcid.org/0000-0003-3844-6457

Catalogue record

Export record

Altmetrics