title: Elevated levels of interferon gamma-inducible protein-10 and epithelial neutrophil-activating peptide-78 in patients with pulmonary sarcoidosis.
abstract: OBJECTIVE
  Interferon gamma-inducible protein (IP)-10 and epithelial neutrophil-activating peptide (ENA)-78 belong to the CXC chemokine family and are important factors in inflammatory lung diseases. In sarcoidosis, the potential role of IP-10 to regulate the migration and activation of T-cells towards sites of sarcoid activity has been suggested.
  
  
  METHODS
  In this study, the concentrations of IP-10 and ENA-78 in the serum and BAL fluid of patients with different stages of active pulmonary sarcoidosis (n=41) and healthy subjects (n=12) were measured by enzyme-linked immunosorbent assay to evaluate the contribution of these CXC chemokines to this disease.
  
  
  RESULTS
  Serum and BAL fluid concentrations of IP-10 and BAL fluid levels of ENA-78 in patients with sarcoidosis were significantly higher than those in control subjects. The serum levels of IP-10 were significantly increased only in patients with stages I and II sarcoidosis, while BAL fluid levels of ENA-78 were increased only in stage III sarcoidosis. In addition, serum concentrations of IP-10 were elevated in patients with extrapulmonary lesions compared with those without such lesions. In patients with sarcoidosis, IP-10 concentrations in BAL fluid correlated with lymphocyte proportions in BAL fluid.
  
  
  CONCLUSIONS
  IP-10 may play an important role in regulating lymphocytes into the lung and that ENA-78 may be associated with lung parenchymal disease in pulmonary sarcoidosis.
authors.affiliation: Second Department of Internal Medicine, Nagasaki University School of Medicine, Nagasaki, Japan.
authors.forename: Kanako
authors.initials: K
authors.lastname: Sugiyama
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Mukae
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Ishii
authors.forename: Tomoyuki
authors.initials: T
authors.lastname: Kakugawa
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Ishimoto
authors.forename: Seiko
authors.initials: S
authors.lastname: Nakayama
authors.forename: Ryo
authors.initials: R
authors.lastname: Shirai
authors.forename: Takeshi
authors.initials: T
authors.lastname: Fujii
authors.forename: Yohei
authors.initials: Y
authors.lastname: Mizuta
authors.forename: Shigeru
authors.initials: S
authors.lastname: Kohno
mesh_terms: D000328:Adult; D000368:Aged; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry / Q000166:cytology; D015496:CD4-Positive T-Lymphocytes / Q000473:pathology; D018414:CD8-Positive T-Lymphocytes / Q000473:pathology; D016022:Case-Control Studies; D002452:Cell Count; D002465:Cell Movement; D054357:Chemokine CXCL10; D054365:Chemokine CXCL5; D019743:Chemokines, CXC / Q000032:analysis / Q000235:genetics / Q000378:metabolism*; D005260:Female; D005786:Gene Expression Regulation; D006801:Humans; D008297:Male; D008875:Middle Aged; D015375:Receptors, Interleukin-2 / Q000032:analysis / Q000235:genetics / Q000378:metabolism; D017565:Sarcoidosis, Pulmonary / Q000378:metabolism* / Q000473:pathology
chemical_list: C486263:CXCL5 protein, human; D054357:Chemokine CXCL10; D054365:Chemokine CXCL5; D019743:Chemokines, CXC; D015375:Receptors, Interleukin-2