Review article: ageing and the neutrophil: no appetite for killing?

Abstract

In the armoury of the immune system developed to combat the various micro-organisms that could invade the host, the neutrophil forms the first line of defence against rapidly dividing bacteria and fungi. However, as humans age they become more susceptible to infection with these microbes and this has been ascribed to a decline in immune status, termed immune senescence. Here we summarize the literature specifically concerning the attenuation of neutrophil function with age and the possible mechanisms underlying their reduced response to infectious agents.

Figure 1

Neutrophil response to infection. The figure shows the adhesion of neutrophils to vascular endothelium, which is mediated by selectins and β₂-integrins, leading to extravasation from blood into the infected tissue. Neutrophils then migrate towards the microbe along a chemotactic gradient, composed of bacterial products and activated complement molecules. The pathogenic organism is ingested by phagocytosis, which is stimulated by bacterial membrane components, complement and/or immunoglobulins, that are recognized by receptors on the neutrophil. Once ingested the microbes are killed by lytic enzymes and reactive oxygen species, and the neutrophil dies by apoptosis. LPS, lipopolysaccharide.