Interleukin-1-Interleukin-17 Signaling Axis Induces Cartilage Destruction and Promotes Experimental Osteoarthritis.
Animals
Arthralgia
/ genetics
Arthritis, Experimental
/ chemically induced
Cartilage, Articular
/ immunology
Cells, Cultured
Chondrocytes
/ drug effects
Humans
Inflammation
/ immunology
Interleukin 1 Receptor Antagonist Protein
/ deficiency
Interleukin-1
/ metabolism
Interleukin-17
/ genetics
Iodoacetic Acid
/ adverse effects
Male
Mice
Mice, Inbred BALB C
Mice, Knockout
Osteoarthritis
/ chemically induced
IL-1 receptor antagonist knockout
inflammation
interleukin-17
intestinal homeostasis
osteoarthritis
Journal
Frontiers in immunology
ISSN: 1664-3224
Titre abrégé: Front Immunol
Pays: Switzerland
ID NLM: 101560960
Informations de publication
Date de publication:
2020
2020
Historique:
received:
29
10
2019
accepted:
31
03
2020
entrez:
21
5
2020
pubmed:
21
5
2020
medline:
30
3
2021
Statut:
epublish
Résumé
Osteoarthritis (OA), which is the most common degenerative joint disorder, has been considered a non-inflammatory disease with abnormal mechanics. Interleukin (IL)-17 is a pleiotropic cytokine involved in inflammatory diseases and their production is driven by the cytokine including IL-1 and IL-23. However, little is known about the mechanism of IL-17 in the development of OA. Here, we investigated the role of IL-17 in the pathogenesis of OA using monosodium iodoacetate (MIA)-injected IL-17 and IL-1 receptor antagonist (IL-1Ra) double-deficient mice. In MIA-injected IL-1Ra KO mice, nociceptive properties, degree of cartilage damage, and the level of inflammatory factors in articular cartilage were increased compared to MIA-injected wild-type mice. Interestingly, the intestinal architecture was impaired in IL-1Ra KO mice compared to wild-type mice and the damage was further exacerbated by MIA injection. Deficiency of IL-17 reduced nociceptive properties and cartilage destruction, as well as inflammation-related factors in MIA-injected IL-1Ra KO mice compared to MIA-injected wild-type mice. Furthermore, IL-17-treated chondrocytes from OA patients showed enhanced expression of catabolic factors that are involved in the destruction of cartilage in OA. IL-17 accelerates the destruction of cartilage and small intestine via regulation of several inflammatory mediators in an OA murine model. These results suggest that IL-17 plays a critical role in the development of OA.
Identifiants
pubmed: 32431699
doi: 10.3389/fimmu.2020.00730
pmc: PMC7214841
doi:
Substances chimiques
IL17A protein, human
0
Il17a protein, mouse
0
Il1rn protein, mouse
0
Interleukin 1 Receptor Antagonist Protein
0
Interleukin-1
0
Interleukin-17
0
Iodoacetic Acid
WF5188V710
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
730Commentaires et corrections
Type : ErratumIn
Informations de copyright
Copyright © 2020 Na, Park, Cho, Kwon, Choi, Jhun, Kim, Park and Cho.
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