2. Academic Validation
  3. Neutrophil extracellular traps and extracellular histones potentiate IL-17 inflammation in periodontitis

Neutrophil extracellular traps and extracellular histones potentiate IL-17 inflammation in periodontitis

  • J Exp Med. 2023 Sep 4;220(9):e20221751. doi: 10.1084/jem.20221751.
Tae Sung Kim 1,  Lakmali M Silva 1 2,  Vasileios Ionas Theofilou 1 3,  Teresa Greenwell-Wild 1,  Lu Li 4,  Drake Winslow Williams 1,  Tomoko Ikeuchi 1,  Laurie Brenchley 1,  NIDCD/NIDCR Genomics and Computational Biology Core,  Thomas H Bugge 2,  Patricia I Diaz 4,  Mariana J Kaplan 5,  Carmelo Carmona-Rivera 5,  Niki M Moutsopoulos 1
Affiliations

Affiliations

  • 1 Oral Immunity and Infection Section, National Institute of Dental and Craniofacial Research , National Institutes of Health, Bethesda, MD, USA.
  • 2 Proteases and Tissue Remodeling Section, National Institute of Dental and Craniofacial Research , National Institutes of Health, Bethesda, MD, USA.
  • 3 Department of Oncology and Diagnostic Sciences, School of Dentistry, University of Maryland, Baltimore, MD, USA.
  • 4 Department of Oral Biology, State University of New York at Buffalo, University at Buffalo, Buffalo, NY, USA.
  • 5 Systemic Autoimmunity Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health , Bethesda, MD, USA.
PMID: 37261457 DOI: 10.1084/jem.20221751
Abstract

Neutrophil infiltration is a hallmark of periodontitis, a prevalent oral inflammatory condition in which Th17-driven mucosal inflammation leads to destruction of tooth-supporting bone. Herein, we document that neutrophil extracellular traps (NETs) are early triggers of pathogenic inflammation in periodontitis. In an established animal model, we demonstrate that neutrophils infiltrate the gingival oral mucosa at early time points after disease induction and expel NETs to trigger mucosal inflammation and bone destruction in vivo. Investigating mechanisms by which NETs drive inflammatory bone loss, we find that extracellular histones, a major component of NETs, trigger upregulation of IL-17/Th17 responses, and bone destruction. Importantly, human findings corroborate our experimental work. We document significantly increased levels of NET complexes and extracellular histones bearing classic NET-associated posttranslational modifications, in blood and local lesions of severe periodontitis patients, in the absence of confounding disease. Our findings suggest a feed-forward loop in which NETs trigger IL-17 immunity to promote immunopathology in a prevalent human inflammatory disease.

Figures
Products
嗨！很高兴为您提供帮助！

尊敬的 MCE 客户您好，
请您选择所在区域，我们将转接对应客服为您服务！

热门区域

A

B

C

F

G

H

J

L

N

Q

S

T

X

Y

Z

热 A B C F G H J L N Q S T X Y Z