Regulatory nexus in inflammation, tissue repair and immune modulation in Crimean-Congo hemorrhagic fever: PTX3, FGF2 and TNFAIP6

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dc.contributor.authorHasbek, Mursit
dc.contributor.authorCakir Kiymaz, Yasemin
dc.contributor.authorOksuz, Caner
dc.contributor.authorErtuerk Zararsiz, Goezde
dc.contributor.authorIpekten, Funda
dc.contributor.authorBuyuktuna, Seyit Ali
dc.date.accessioned2026-04-04T13:32:59Z
dc.date.available2026-04-04T13:32:59Z
dc.date.issued2025
dc.departmentİnönü Üniversitesi
dc.description.abstractObjectives This study emphasizes the importance of determining the serum levels of pentraxin-3 (PTX3), fibroblast growth factor-2 (FGF2), and tumor necrosis factor-stimulated gene-6 (TNFAIP6) in patients with Crimean-Congo hemorrhagic fever (CCHF).Methods This prospective study involved 30 confirmed CCHF patients and 30 healthy controls. Serum concentrations of PTX3, FGF2, and TNFAIP6 were quantified utilizing a quantitative sandwich ELISA method.Results CCHF patients exhibited markedly elevated PTX3 levels, reflecting an acute inflammatory response. As a long pentraxin, PTX3 functions as a pattern recognition receptor that activates the complement system to aid in pathogen clearance. Additionally, FGF2 levels were significantly increased, indicating a potential role in repairing endothelial damage. Known for promoting angiogenesis and immune regulation, FGF2 may counteract endothelial dysfunction induced by CCHF. Conversely, TNFAIP6 levels were lower in patients, possibly due to shifts in cytokine activity that suppress its anti-inflammatory and extracellular matrix-regulating effects, potentially leading to greater tissue injury.Conclusions The dysregulation of PTX3, FGF2, and TNFAIP6 in CCHF patients signifies a disrupted equilibrium in inflammatory and vascular response mechanisms. This triad of biomarkers could serve as a valuable tool for assessing the severity of CCHF and may present therapeutic targets for modulating inflammation and mitigating endothelial damage. Achieving a balance among PTX3, FGF2, and TNFAIP6 could be instrumental in alleviating disease complications, thereby suggesting a potential therapeutic strategy for managing CCHF effectively.
dc.identifier.doi10.1515/tjb-2025-0050
dc.identifier.endpage394
dc.identifier.issn0250-4685
dc.identifier.issn1303-829X
dc.identifier.issue3
dc.identifier.orcid0000-0002-3944-4608
dc.identifier.orcid0000-0002-5495-7540
dc.identifier.orcid0000-0001-6518-7361
dc.identifier.orcid0000-0002-5217-8607
dc.identifier.startpage388
dc.identifier.urihttps://doi.org/10.1515/tjb-2025-0050
dc.identifier.urihttps://hdl.handle.net/11616/108855
dc.identifier.volume50
dc.identifier.wosWOS:001494808500001
dc.identifier.wosqualityQ4
dc.indekslendigikaynakWeb of Science
dc.language.isoen
dc.publisherWalter De Gruyter Gmbh
dc.relation.ispartofTurkish Journal of Biochemistry-Turk Biyokimya Dergisi
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/openAccess
dc.snmzKA_WOS_20250329
dc.subjectCrimean-Congo hemorrhagic fever
dc.subjectpentraxin-3
dc.subjectfibroblast growth factor-2
dc.subjecttumor necrosis factor-stimulated gene-6
dc.subjectinflammation
dc.titleRegulatory nexus in inflammation, tissue repair and immune modulation in Crimean-Congo hemorrhagic fever: PTX3, FGF2 and TNFAIP6
dc.typeArticle

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