Open AccessAirway epithelium expresses interleukin‐18
Author(s) -
Cameron L.a.,
Taha R.a.,
Tsicopoulos A,
Kurimoto M,
Olivenstein R.,
Wallaert B,
Minshall E.m.,
Hamid Q.a.
Publication year - 1999
Publication title -
european respiratory journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.021
H-Index - 241
eISSN - 1399-3003
pISSN - 0903-1936
DOI - 10.1034/j.1399-3003.1999.14c12.x
Subject(s) - cytokine , ovalbumin , respiratory epithelium , in situ hybridization , epithelium , immunology , biology , lipopolysaccharide , interleukin 4 , interleukin , peripheral blood mononuclear cell , messenger rna , medicine , pathology , immune system , in vitro , biochemistry , gene
Interleukin(IL)‐18 is an interferon (IFN)‐γ‐inducing cytokine suggested to be important in regulating inflammatory responses. This study investigated the pulmonary expression of IL‐18 under conditions characterized by T‐helper (Th)1 (lipopolysaccharide (LPS) treatment/sarcoidosis) and Th2 (ovalbumin (OVA) challenge/asthma) cytokine production. In situ hybridization and immunocytochemistry were used to determine the number of cells expressing IL‐18, IFN‐γ, IL‐5 and major basic protein (MBP) within lung tissue from Balb/c mice stimulated with LPS, OVA and in normal control mice. Bronchial biopsies from patients with sarcoidosis, asthma and control individuals were also examined. IL‐18 was localized primarily to airway epithelium and mononuclear cells. Constitutive expression was observed within the lungs of control mice. Animals challenged with LPS exhibited more IL‐18 messenger ribonucleic acid (mRNA)‐positive and IFN‐γ immunoreactive cells, compared to control mice (p<0.01). OVA‐challenged mice had fewer IL‐18 mRNA positive and more IL‐5 and MBP immunoreactive cells, compared to control mice (p<0.01). Similarly, constitutive expression of IL‐18 protein was observed within the airway epithelium of control individuals, with more positive cells found within sarcoidosis tissue (p<0.01) and fewer within asthmatic tissue (p<0.01), compared to controls. These results demonstrate the expression of interleukin‐18 within airway epithelium and the regulation of this cytokine under conditions of both T‐helper1 and T‐helper2 cytokine production.