Format

Send to

Choose Destination
Cell Tissue Res. 2018 Mar;371(3):455-471. doi: 10.1007/s00441-017-2731-8. Epub 2017 Nov 29.

Armed for destruction: formation, function and trafficking of neutrophil granules.

Author information

1
Department of Microbiology and Immunology and the Center for Human Immunology, The University of Western Ontario, London, ON, Canada.
2
Department of Microbiology and Immunology and the Center for Human Immunology, The University of Western Ontario, London, ON, Canada. bheit@uwo.ca.

Abstract

Neutrophils respond nearly instantly to infection, rapidly deploying a potent enzymatic and chemical arsenal immediately upon entering an infected site. This capacity for rapid and potent responses is endowed by stores of antimicrobial proteins contained in readily mobilizable granules. These granules contain the proteins necessary to mediate the recruitment, chemotaxis, antimicrobial function and NET formation of neutrophils. Four granule types exist, and are sequentially deployed as neutrophils enter infected sites. Secretory vesicles are released first, enabling recruitment of neutrophils out of the blood. Next, specific and gelatinase granules are released to enable neutrophil migration and begin the formation of an antimicrobial environment. Finally, azurophilic granules release potent antimicrobial proteins at the site of infection and into phagosomes. The step-wise mobilization of these granules is regulated by calcium signaling, while specific trafficking regulators and membrane fusion complexes ensure the delivery of granules to the correct subcellular site. In this review, we describe neutrophil granules from their formation through to their deployment at the site of infection, focusing on recent developments in our understanding of the signaling pathways and vesicular trafficking mechanisms which mediate neutrophil degranulation.

KEYWORDS:

Calcium; Degranulation; GTPase; Granulopoiesis; Neutrophil; Vesicular traffic

PMID:
29185068
DOI:
10.1007/s00441-017-2731-8
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Springer
Loading ...
Support Center