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Neutrophils sense microbe size and selectively release neutrophil extracellular traps in response to large pathogens.

Authors
  • Branzk, Nora
  • Lubojemska, Aleksandra
  • Hardison, Sarah E
  • Wang, Qian
  • Gutierrez, Maximiliano G
  • Brown, Gordon D
  • Papayannopoulos, Venizelos
Type
Published Article
Journal
Nature Immunology
Publisher
Springer Nature
Publication Date
Nov 01, 2014
Volume
15
Issue
11
Pages
1017–1025
Identifiers
DOI: 10.1038/ni.2987
PMID: 25217981
Source
Medline
License
Unknown

Abstract

Neutrophils are critical for antifungal defense, but the mechanisms that clear hyphae and other pathogens that are too large to be phagocytosed remain unknown. We found that neutrophils sensed microbe size and selectively released neutrophil extracellular traps (NETs) in response to large pathogens, such as Candida albicans hyphae and extracellular aggregates of Mycobacterium bovis, but not in response to small yeast or single bacteria. NETs were fundamental in countering large pathogens in vivo. Phagocytosis via dectin-1 acted as a sensor of microbe size and prevented NET release by downregulating the translocation of neutrophil elastase (NE) to the nucleus. Dectin-1 deficiency led to aberrant NET release and NET-mediated tissue damage during infection. Size-tailored neutrophil responses cleared large microbes and minimized pathology when microbes were small enough to be phagocytosed.

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