Exploring Chemokines and Soluble Adhesion Molecules in Mustard Lung Pathogenesis Publisher Pubmed



Rezaei A¹ ; Pourfarzam S² ; Jamali T³ ; Mohammadi NG⁴ ; Andalib A¹ ; Hassan ZM⁵ ; Ayubi F³ ; Ghazanfari T^{3, 6} Show Affiliations
Source: International Immunopharmacology Published:2025

Abstract

Sulfur mustard (SM), functioning as an alkylating agent, plays a significant role in developing respiratory system pathologies. This study aimed to evaluate serum concentrations of chemokines and soluble adhesion molecules in serious mustard lung (ML) patients 25–30 years after exposure to SM, exploring their roles in ML pathogenesis and disease severity. The study included 275 individuals exposed to SM and 64 unexposed individuals as controls. Serum samples were collected and clinical evaluations categorized disease severity and pulmonary pathogenesis. Serum levels of MCP-1/CCL2, RANTES/CCL5, CX3CL1, CXCL12s, P-selectin, sL-selectin, sE-selectin, sICAM-1 levels were measured using ELISA kits, and mRNA expression of CXCR4 in whole blood was determined via real-time PCR. Data analysis included comparisons between groups. SM-exposed individuals exhibited significantly higher MCP-1/CCL2 and RANTES/CCL5 levels, with decreased CX3CL1 levels compared to controls. CXCL12, selectins, sICAM-1 levels, and the expression level of CXCR4 showed no significant differences. Changes in some of the mentioned factors were observed, along with changes in the severity of the disease, suggesting potential roles in ML progression. The findings suggest a complex interplay of immune responses in ML pathogenesis, with elevated MCP-1/CCL2 and RANTES/CCL5 potentially contributing to inflammation, while decreased CX3CL1 levels and unchanged CXCL12 and CXCR4 may impair immune responses and tissue repair mechanisms. The unique chemokine and adhesion molecule profile observed in SM-exposed subgroups suggests ML as a differentiated pulmonary disease requiring further investigation into its pathogenesis and relationship with inflammatory disorders. © 2025