Role of Interleukin-17 family cytokines in disease severity of patients with knee osteoarthritis.

Inflammation Interleukin-17 Interleukin-25 Knee osteoarthritis Obesity

Journal

Advances in rheumatology (London, England)
ISSN: 2523-3106
Titre abrégé: Adv Rheumatol
Pays: England
ID NLM: 101734172

Informations de publication

Date de publication:
24 Jan 2024
Historique:
received: 22 03 2023
accepted: 09 01 2024
medline: 25 1 2024
pubmed: 25 1 2024
entrez: 24 1 2024
Statut: epublish

Résumé

Interleukin-17 (IL-17) family plays a role in the pathogenesis of knee osteoarthritis (KOA) by contributing to the inflammatory and destructive processes in the affected joint. This study aimed to measure levels of IL-17 A and IL-25 (IL-17E) in serum of KOA patients and determine their roles in the disease severity of patients. In this, 34 patients with KOA and 30 age and sex-matched healthy subjects (HS) were enrolled. Patients were categorized based on their Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC), Visual Analog Scale (VAS), and Body Mass Index (BMI) scores. The enzyme-linked immunosorbent assay (ELISA) technique was employed to measure serum levels of IL-17 A and IL-25. Level of IL-25 was significantly higher (P < 0.0001) in the KOA subjects than HS. IL-17 A level was significantly higher in KOA cases with WOMAC < 40 (P < 0.0001) in comparison to HS. IL-25 level was significantly higher in the KOA cases with WOMAC < 40 (P < 0.0001) and with WOMAC ≥ 40 (P < 0.0001) compared to HS. IL-17 A concentration was significantly higher in the KOA cases with VAS < 5 (P < 0.0001) compared to HS. IL-25 level was significantly higher in the KOA cases with VAS < 5 (P < 0.0001) and with VAS ≥ 5 (P < 0.0001) in comparison to HS. KOA patients with BMI ≥ 30 had significantly higher IL-17 A and IL-25 concentration in comparison to HS. The serum level of IL-25 in KOA patients is increased probably due to negative controlling feedback on inflammatory responses, which can be associated with obesity and disease activity.

Sections du résumé

BACKGROUND BACKGROUND
Interleukin-17 (IL-17) family plays a role in the pathogenesis of knee osteoarthritis (KOA) by contributing to the inflammatory and destructive processes in the affected joint. This study aimed to measure levels of IL-17 A and IL-25 (IL-17E) in serum of KOA patients and determine their roles in the disease severity of patients.
METHODS METHODS
In this, 34 patients with KOA and 30 age and sex-matched healthy subjects (HS) were enrolled. Patients were categorized based on their Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC), Visual Analog Scale (VAS), and Body Mass Index (BMI) scores. The enzyme-linked immunosorbent assay (ELISA) technique was employed to measure serum levels of IL-17 A and IL-25.
RESULTS RESULTS
Level of IL-25 was significantly higher (P < 0.0001) in the KOA subjects than HS. IL-17 A level was significantly higher in KOA cases with WOMAC < 40 (P < 0.0001) in comparison to HS. IL-25 level was significantly higher in the KOA cases with WOMAC < 40 (P < 0.0001) and with WOMAC ≥ 40 (P < 0.0001) compared to HS. IL-17 A concentration was significantly higher in the KOA cases with VAS < 5 (P < 0.0001) compared to HS. IL-25 level was significantly higher in the KOA cases with VAS < 5 (P < 0.0001) and with VAS ≥ 5 (P < 0.0001) in comparison to HS. KOA patients with BMI ≥ 30 had significantly higher IL-17 A and IL-25 concentration in comparison to HS.
CONCLUSIONS CONCLUSIONS
The serum level of IL-25 in KOA patients is increased probably due to negative controlling feedback on inflammatory responses, which can be associated with obesity and disease activity.

Identifiants

DOI: 10.1186/s42358-024-00351-5 PMID: 38268022
pubmed: 38268022
doi: 10.1186/s42358-024-00351-5
pii: 10.1186/s42358-024-00351-5
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

11

Informations de copyright

© 2024. The Author(s).

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Auteurs

Zahra Kamiab (Z)

Department of Community Medicine, School of Medicine, Rafsanjan University of Medical Sciences, Rafsanjan, Iran, Rafsanjan, Iran.

Hossein Khorramdelazad (H)

Department of Immunology, Faculty of Medicine, Rafsanjan University of Medical Sciences, Rafsanjan, Iran, Rafsanjan, Iran.

Mehdi Kafi (M)

Student Research Committee, Rafsanjan University of Medical Sciences, Rafsanjan, Iran, Kerman, Iran.

Abdollah Jafarzadeh (A)

Department of Immunology, School of Medicine, Kerman University of Medical Sciences, Kerman, Iran, Rafsanjan, Iran.
Molecular Medicine Research Center, Research Institute of Basic Medical Sciences, Rafsanjan University of Medical Sciences, Rafsanjan, Iran, Tehran, Iran.

Vahid Mohammadi-Shahrokhi (V)

Department of Immunology, Faculty of Medicine, Rafsanjan University of Medical Sciences, Rafsanjan, Iran, Rafsanjan, Iran.
Immunology of Infectious Diseases Research Center, Research Institute of Basic Medical Sciences, Rafsanjan University of Medical Sciences, Rafsanjan, Iran, Rafsanjan, Iran.

Zahra Bagheri-Hosseinabadi (Z)

Department of Clinical Biochemistry, School of Medicine, Rafsanjan University of Medical Sciences, Rafsanjan, Iran, Rafsanjan, Iran.

Pooya Saeed Askari (P)

Student Research Committee, Rafsanjan University of Medical Sciences, Rafsanjan, Iran, Kerman, Iran.
Department of Internal Medicine,, Faculty of Medicine, Molecular Medicine Research Center, Institute of Basic Medical Sciences Research, Rafsanjan University of Medical Sciences, Rafsanjan, Iran, Rafsanjan, Iran.

Mitra Abbasifard (M)

Immunology of Infectious Diseases Research Center, Research Institute of Basic Medical Sciences, Rafsanjan University of Medical Sciences, Rafsanjan, Iran, Rafsanjan, Iran. dr.abbasifard.m@gmail.com.
Department of Internal Medicine, Ali-Ibn Abi-Talib Hospital, School of Medicine, Rafsanjan University of Medical Sciences, Rafsanjan, Iran, Rafsanjan, Iran. dr.abbasifard.m@gmail.com.
ORCID: 0000-0001-8149-8549

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