Cytokine Analysis in Patients with Different Stages of Thromboangiitis Obliterans

Abstract

Background: Studies suggest that cytokines are involved in the development of both inflammatory disorders and vascular diseases. Objective: The changes in transforming growth factor β (TGFβ), interleukin 6 (IL6), tumor necrosis factor α (TNFα), and interferon γ (IFNγ) with the progression of the thromboangiitis obliterans (TAO) symptomswereinvestigated in this research. Methods: This study included 80 patients with TAO, who were selected from the Vascular and Endovascular Research Center in Alavi Hospital between 2012 and 2016. They were then categorized into three groups: mild (migratory thrombophlebitis, cold sensitivity or Raynaud's phenomenon, and skin discoloration), moderate (chronic ulcers, claudication, and burning pain of the feet at night), and severe (pain at rest and spontaneous gangrene) symptoms. The serum levels of TGFβ, IL6, TNFα, and IFNγwere determinedby the ELISA method and compared among the groups. Results: The first three predominant symptoms were pulse disorder (n = 76, 95.00%), cold intolerance (n = 61, 76.25%), and claudication (n = 59, 73.75%). A comparison of the analysis of covariance (ANCOVA) revealed that both TGFβ and IL6 were dysregulatedas the severity of the symptoms increased from the moderate to the severe stages; however, such changes were not significant(p > 0.05). In the multiple logistic regression model, increased TNFαlevelswere seen in the presence of the moderatesymptoms as compared to the severe ones (p < 0.05). Conclusion: It could be concluded that TNFα, as part of the defining cytokine-production profile of Thelper cells, can be significantly involved in the progression of TAO from the moderate to the severe stages.

Iliac crest bone distraction surgery for the treatment of thromboangiitis obliterans of lower limbs: A cohort-prospective preliminary study

“…The manifestation of resting pain, the underlying mechanisms of which are still incompletely understood, stands as a pivotal symptom in patients with TAO. Current literature presents several potential causative factors of rest pain, such as circulatory disorders, neuroin ammatory agents, in ammation-mediated vascular endothelial dysfunction, and other immunomodulated mechanisms [28][29][30]. The widely accepted view is that TAO is postulated as an immunomodulated disease due to abnormal immune system activation inducing in ammatory reactions, possibly contributing to pain generation [31,32].…”

“…Current literature presents several potential causative factors of rest pain, such as circulatory disorders, neuroin ammatory agents, in ammation-mediated vascular endothelial dysfunction, and other immunomodulated mechanisms [28][29][30]. The widely accepted view is that TAO is postulated as an immunomodulated disease due to abnormal immune system activation inducing in ammatory reactions, possibly contributing to pain generation [31,32]. IL-6, a crucial pro-in ammatory cytokine produced and released by macrophages, is a central mediator orchestrating immune and in ammatory responses [33].…”

Baiying qingmai formulation ameliorates thromboangiitis obliterans by inhibiting HMGB1/RAGE/NF-κB signaling pathways

“…Endothelial cells, platelets, and leukocytes are the main components involved in the vascular inflammatory response and thrombosis. Several pro-inflammatory cytokines including IL-6, TNF-α, HMGB1, and IL-1β are abnormally high in the blood of Frontiers in Pharmacology frontiersin.org patients with TAO (Fazeli et al, 2021;Shapouri-Moghaddam et al, 2021). An increase in IL-6 issues a warning signal during tissue damage or infectious lesions.…”

“…HMGB1 elicits pro-inflammatory responses in various cells and is involved in the development of arteriosclerosis and systemic vasculitis, including Kawasaki syndrome, Churg Strauss syndrome, and Henoch-Schonlein purpura ( Kang et al, 2014 ). It induces the release of inflammatory cytokines from neutrophils and macrophages ( Al-Kuraishy et al, 2022 ), leads to IL-6 and TNF secretion by monocytes ( Liu et al, 2018 ; Wei et al, 2018 ), and stimulates the production of TNF-α ( Shapouri-Moghaddam et al, 2021 ), intercellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1) by endothelial cells ( Fiuza et al, 2003 ). Therefore, HMGB1 may be a potential key target in the treatment of TAO ( De Caridi et al, 2016 ; Mousazadeh et al, 2019 ).…”