Inhibitory role of interleukin-10 in the cutaneous reverse Arthus reaction.


Journal

The Journal of dermatology
ISSN: 1346-8138
Titre abrégé: J Dermatol
Pays: England
ID NLM: 7600545

Informations de publication

Date de publication:
Feb 2021
Historique:
received: 25 02 2020
accepted: 13 09 2020
pubmed: 17 10 2020
medline: 15 5 2021
entrez: 16 10 2020
Statut: ppublish

Résumé

The formation and deposition of immune complexes (IC) containing immunoglobulin (Ig)G antibodies induces an acute inflammatory response with tissue injury. One of the experimental models of IC-related vasculitis is the cutaneous reverse passive Arthus reaction, in which IgG antibodies are injected i.d., followed immediately by the i.v. application of the corresponding antigen. This reaction is characterized by edema, hemorrhage and neutrophil infiltration. To assess the role of the anti-inflammatory cytokine interleukin (IL)-10 in IC-related vasculitis, we investigated the cutaneous Arthus reaction using IL-10 knockout (IL-10KO) mice. Edema, which was quantified macroscopically by measuring the vascular leakage of Evans blue dye at 4 h after IC challenge, was significantly increased in IL-10KO mice compared with wild-type mice. In addition, hemorrhage, which was assessed by the average diameter of purpuric spots at 8 h after IC challenge, was enhanced significantly in IL-10KO mice compared with wild-type mice. Histological examination showed that the number of extravascular neutrophils was significantly increased in IL-10KO mice compared with wild-type mice at 4 and 8 h after IC challenge. Analysis of pro-inflammatory cytokine mRNA expression showed that IL-6 mRNA levels were significantly increased in IL-10KO mice compared with wild-type mice at 4 and 8 h after IC challenge. These results showed that IC-induced inflammation and vascular damage were significantly enhanced in the absence of IL-10. Thus, IL-10 may limit tissue disruption by suppressing the excessive infiltration of neutrophils and cytokine expression in a mouse model of type III vasculitis.

Identifiants

pubmed: 33063335
doi: 10.1111/1346-8138.15641
doi:

Substances chimiques

Antigen-Antibody Complex 0
Cytokines 0
Interleukin-10 130068-27-8

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

219-222

Subventions

Organisme : Ministry of Education, Culture, Sports, Science and Technology of Japan

Informations de copyright

© 2020 Japanese Dermatological Association.

Références

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Auteurs

Nobuko Ishiura (N)

Department of Regenerative Medicine, Research Institute, National Center for Global Health and Medicine, Tokyo, Japan.
Department of Dermatology, Japan Community Health-care Organization Tokyo Shinjuku Medical Center, Tokyo, Japan.

Koichi Yanaba (K)

Department of Dermatology, The Jikei University Katsushika Medical Center, Tokyo, Japan.

Kiyoko Nashiro (K)

Department of Regenerative Medicine, Research Institute, National Center for Global Health and Medicine, Tokyo, Japan.

Mari Kudo (M)

Department of Dermatology, National Center for Global Health and Medicine, Tokyo, Japan.

Taeko Goto (T)

Department of Dermatology, National Center for Global Health and Medicine, Tokyo, Japan.

Hitoshi Okochi (H)

Department of Regenerative Medicine, Research Institute, National Center for Global Health and Medicine, Tokyo, Japan.

Shinichi Sato (S)

Department of Dermatology, Tokyo University Graduate School of Medicine, Tokyo, Japan.

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