IL-36 signaling pathway dysregulation in Crimean–Congo hemorrhagic fever virus patients: A potential therapeutic avenue


Doğan K., Büyüktuna S. A.

Journal of Medical Virology, cilt.96, sa.1, 2024 (SCI-Expanded) identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 96 Sayı: 1
  • Basım Tarihi: 2024
  • Doi Numarası: 10.1002/jmv.29347
  • Dergi Adı: Journal of Medical Virology
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, BIOSIS, CAB Abstracts, Veterinary Science Database
  • Anahtar Kelimeler: Crimean–Congo hemorrhagic fever virus, cytokines, interleukin
  • Sivas Cumhuriyet Üniversitesi Adresli: Hayır

Özet

Crimean–Congo hemorrhagic fever (CCHF) is a severe viral disease. The scientific literature is growing, emphasizing the significance of the interleukin (IL)-36 family in the proinflammatory signaling pathway. However, to date, no research has explored the potential of IL-36 family members as biomarkers in CCHF. This study aims to bridge this gap by evaluating IL-36α, IL-36β, and IL-36γ levels in CCHF patients and healthy controls and investigating their association with disease severity and prognosis. Sixty confirmed CCHF patients and 29 healthy controls were enrolled in this case-control study. Serum levels of IL-36α, IL-36β, and IL-36γ were measured using enzyme-linked immunosorbent assays. Significantly higher levels of IL-36α and IL-36β were observed in CCHF patients compared to healthy controls (p < 0.05). However, no statistically significant changes were found in IL-36γ levels between the two groups. Among the CCHF patients, those who did not survive exhibited significantly elevated IL-36α and IL-36γ levels compared to survivors (p < 0.01). Positive correlations were identified between IL-36α and IL-36γ levels with activated partial thromboplastin time, and D-dimer (p < 0.01). Conversely, platelet levels showed a negative correlation with IL-36α and IL-36γ levels (p < 0.01). The increased levels of IL-36α, IL-36β, and IL-36γ in patients indicate their participation in proinflammatory reactions in CCHF patients. Understanding the role of IL-36 family members in CCHF pathogenesis could offer valuable insights into disease progression and facilitate the development of targeted therapeutic strategies.