title: Elevated levels of MCP-1, MIP-alpha and MIP-1 beta in the bronchoalveolar lavage (BAL) fluid of patients with mustard gas-induced pulmonary fibrosis.
abstract: OBJECTIVE
  Role of chemokines in the pathogenesis of pulmonary fibrosis (PF) due to sulfur mustard (SM) gas inhalation.
  
  
  METHODS
  18 veterans with SM gas-induced PF, 15 patients with IPF and 18 normal as controls.
  
  
  METHODS
  Chest roentgenograms, PFTs, the percentage DLCO, high-resolution CT scans of the chest, and analyses of BAL fluids for chemokines (MCP-1, MIP-1 alpha, and MIP-1 beta) were performed in all cases.
  
  
  RESULTS
  There were significant differences in chemokines (MCP-1, MIP-1 alpha, and MIP-1 beta) levels of BAL fluid between patients with PF and healthy controls (p<0.0006). MCP-1 and MIP-1 alpha levels in BAL fluid correlate only with the percentage and the absolute number lymphocytes of the BAL fluid in patients with PF due to SM gas inhalation (p=0.0006/p=0.03; p=0.04/p=0.02; respectively). The BAL fluid level of MIP-alpha in SM gas-induced PF was significantly correlated with the number of lymphocytes (r=-0.56, p=0.01), neutrophils (r=-0.50, p=0.03) and eosinophils (r=-0.49, p=0.03). A significant negative correlation was observed between the percentage of Dlco and MCP-1 and MIP-1 alpha levels in BAL fluid in patients with PF (r=-0.65, p=0.003; r=-0.48, p=0.04; respectively).
  
  
  CONCLUSIONS
  Neutrophils alveolitis, presence of eosinophils, and higher concentrations of interleukin MCP-1, MIP-1 alpha, and MIP-1 beta in BAL fluid are associated with the development of fibrosis in SM victims.
authors.affiliation: Department of Internal Medicine, Section of Pulmonary Diseases, Shiraz University of Medical Sciences, Shiraz, Iran. lungdep@pearl.sums.ac.ir
authors.forename: Ali
authors.initials: A
authors.lastname: Emad
authors.forename: Vahid
authors.initials: V
authors.lastname: Emad
mesh_terms: D000328:Adult; D001992:Bronchoalveolar Lavage Fluid / Q000166:cytology / Q000276:immunology*; D016022:Case-Control Studies; D002452:Cell Count; D002619:Chemical Warfare Agents / Q000633:toxicity*; D018932:Chemokine CCL2 / Q000032:analysis* / Q000276:immunology; D054405:Chemokine CCL3 / Q000032:analysis* / Q000276:immunology; D054407:Chemokine CCL4 / Q000032:analysis*; D004804:Eosinophils / Q000166:cytology; D006801:Humans; D008214:Lymphocytes / Q000166:cytology; D016676:Macrophages, Alveolar / Q000166:cytology; D009151:Mustard Gas / Q000633:toxicity*; D009504:Neutrophils / Q000166:cytology; D011658:Pulmonary Fibrosis / Q000139:chemically induced* / Q000276:immunology
chemical_list: C111835:CCL2 protein, human; C515429:CCL3 protein, human; C066507:CCL4 protein, human; D002619:Chemical Warfare Agents; D018932:Chemokine CCL2; D054405:Chemokine CCL3; D054407:Chemokine CCL4; D009151:Mustard Gas