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Exploring chemokines and soluble adhesion molecules in mustard lung pathogenesis
Abbas Rezaei1, Shahryar Pourfarzam2, Tahereh Jamali3
1Department of Immunology, Faculty of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran.
International Immunopharmacology
|February 9, 2025
Summary
Long-term sulfur mustard (SM) exposure elevates inflammatory chemokines MCP-1/CCL2 and RANTES/CCL5, while decreasing CX3CL1, impacting mustard lung (ML) pathogenesis and immune response. These findings highlight ML as a distinct pulmonary condition.
Area of Science:
- Toxicology
- Immunology
- Pulmonology
Background:
- Sulfur mustard (SM) is an alkylating agent causing significant respiratory pathologies.
- Mustard lung (ML) is a severe, long-term consequence of SM exposure.
- Understanding the chronic immune response in ML is crucial for pathogenesis insights.
Purpose of the Study:
- To evaluate serum chemokine and soluble adhesion molecule levels in individuals with chronic ML.
- To explore the role of these molecules in ML pathogenesis and disease severity 25-30 years post-exposure.
- To investigate potential differences in immune markers between SM-exposed individuals and controls.
Main Methods:
- Serum samples from 275 SM-exposed individuals and 64 controls were analyzed.
- Levels of MCP-1/CCL2, RANTES/CCL5, CX3CL1, CXCL12, P-selectin, sL-selectin, sE-selectin, and sICAM-1 were measured using ELISA.
- mRNA expression of CXCR4 in whole blood was determined via real-time PCR.
Main Results:
- SM-exposed individuals showed significantly higher MCP-1/CCL2 and RANTES/CCL5 levels.
- Decreased serum levels of CX3CL1 were observed in the SM-exposed group.
- No significant differences were found in CXCL12, selectins, sICAM-1, or CXCR4 expression.
Conclusions:
- Elevated MCP-1/CCL2 and RANTES/CCL5 suggest a role in chronic ML inflammation.
- Reduced CX3CL1 and unchanged CXCL12/CXCR4 may indicate impaired immune response and tissue repair.
- The distinct molecular profile supports ML as a differentiated pulmonary disease requiring further research.
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