ADAM10 inhibits the interaction between IL-17 and HMGB1 in Buerger's disease.
Eur Rev Med Pharmacol Sci
; 25(11): 4051-4063, 2021 06.
Article
in En
| MEDLINE
| ID: mdl-34156683
ABSTRACT
OBJECTIVE:
Buerger's disease is a rare disease that causes critical limb ischemia; however, the underlying pathophysiological mechanism remains unclear. Therefore, we investigated the interaction between interleukin (IL)-17 and high-mobility group protein B 1 (HMGB1) and determined whether A disintegrin and metalloproteinase 10 (ADAM10) inhibit this interaction. PATIENTS ANDMETHODS:
The study population included 15 patients with Buerger's disease and 10 healthy donors without a history of giving peripheral blood samples. Cytokine levels were measured using a luminex multiplex assay in plasma. Flow cytometry was used to analyze the subtypes of helper T (Th) cells among peripheral blood mononuclear cells (PBMCs). The effect of ADAM10 on PBMCs was analyzed in vitro.RESULTS:
The levels of inflammatory cytokines and production of pathogenic Th cells were found to be higher in Korean patients with Buerger's disease. IL-17 treatment induced HMGB1 associated molecules. HMGB1 also induced IL-17 and Th17 associated transcription factors in Buerger's patients. We observed that ADAM10 regulates the interaction between IL-17 and HMGB1 via advanced glycation end products (RAGE)/nuclear factor-kappa B (NF-kB) pathway in patients with Buerger's disease.CONCLUSIONS:
This study suggests that IL-17 and HMGB1 cytokines contribute to the pathogenesis of Buerger's disease. These results indicate that ADAM10 alleviates inflammation in Buerger's disease via the HMGB1 and RAGE/NF-κB signaling pathway and provides insights into the molecular basis of and a potential therapeutic strategy for Buerger's disease.
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Main subject:
Thromboangiitis Obliterans
/
Cytokines
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HMGB1 Protein
Limits:
Adult
/
Female
/
Humans
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Male
/
Middle aged
Language:
En
Journal:
Eur Rev Med Pharmacol Sci
Journal subject:
FARMACOLOGIA
/
TOXICOLOGIA
Year:
2021
Document type:
Article