Hyaluronan primes the oxidative burst in human neutrophils.
Apoptosis
/ drug effects
Cytokines
/ metabolism
Humans
Hyaluronic Acid
/ metabolism
Inflammation Mediators
/ metabolism
Leukocytes, Mononuclear
/ drug effects
NADPH Oxidases
/ metabolism
Neutrophils
/ drug effects
Oxidation-Reduction
Phosphorylation
Reactive Oxygen Species
/ metabolism
Respiratory Burst
/ immunology
Signal Transduction
NADPH-oxidase
glycosaminoglycans
innate immunity
peripheral blood cells
reactive oxygen species
Journal
Journal of leukocyte biology
ISSN: 1938-3673
Titre abrégé: J Leukoc Biol
Pays: England
ID NLM: 8405628
Informations de publication
Date de publication:
08 2020
08 2020
Historique:
received:
26
08
2019
revised:
18
02
2020
accepted:
08
04
2020
pubmed:
19
5
2020
medline:
15
12
2020
entrez:
19
5
2020
Statut:
ppublish
Résumé
Hyaluronan (HA) is a glycosaminoglycan that in its natural, high molecular mass (HMM) form, promotes tissue repair and homeostasis. With inflammation, HA metabolism and HMM HA fragmentation to low molecular mass (LMM) forms is greatly enhanced. Considerable evidence suggests that LMM HA may act as a damage-associated molecular pattern to initiate innate immune responses. However, the responsiveness of myeloid cells to LMM HA is controversial and largely unknown for neutrophils. Peripheral blood cells from healthy donors were incubated ex vivo with pharmaceutical grade HA of different molecular mass (HMM, LMM, and HA fragments <10 kDa). Key innate immune functions were assessed, namely production of cytokines and reactive oxygen species release (ROS), granule mobilization, and apoptosis. None of the tested sizes of HA altered cytokine production by PBMC and neutrophils. Also, HA had no effect on neutrophil granule mobilization and apoptosis. In contrast, HA primed neutrophils for rapid and robust release of ROS in response to a secondary stimulus (N-formyl-methionyl-leucyl phenylalanine). Priming occurred within 20 min of exposure to HA and was similar for all tested molecular mass. The observed effect was independent of granule mobilization and associated with the activation of intracellular signaling pathways involving Src family kinases, glycogen synthase kinase-3, and the proline-rich Akt substrate of 40 kDa. Our findings provide new evidence that HA, irrespective of molecular mass, is a specific priming agent of the neutrophil oxidative burst, which is a critical, early component of an innate immune response.
Identifiants
pubmed: 32421905
doi: 10.1002/JLB.3MA0220-216RR
doi:
Substances chimiques
Cytokines
0
Inflammation Mediators
0
Reactive Oxygen Species
0
Hyaluronic Acid
9004-61-9
NADPH Oxidases
EC 1.6.3.-
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
705-713Informations de copyright
©2020 Society for Leukocyte Biology.
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