title: Airway epithelium expresses interleukin-18.
abstract: Interleukin (IL)-18 is an interferon (IFN)-gamma-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-gamma, 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-gamma 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.
authors.affiliation: Meakins-Christie Laboratories and Montreal Chest Institute Research Center, McGill University, Quebec, Canada.
authors.forename: L A
authors.initials: LA
authors.lastname: Cameron
authors.forename: R A
authors.initials: RA
authors.lastname: Taha
authors.forename: A
authors.initials: A
authors.lastname: Tsicopoulos
authors.forename: M
authors.initials: M
authors.lastname: Kurimoto
authors.forename: R
authors.initials: R
authors.lastname: Olivenstein
authors.forename: B
authors.initials: B
authors.lastname: Wallaert
authors.forename: E M
authors.initials: EM
authors.lastname: Minshall
authors.forename: Q A
authors.initials: QA
authors.lastname: Hamid
mesh_terms: D000328:Adult; D000368:Aged; D000818:Animals; D001249:Asthma / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D001798:Blood Proteins / Q000235:genetics / Q000378:metabolism; D047091:Eosinophil Granule Proteins; D004847:Epithelial Cells / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology; D005260:Female; D006801:Humans; D007124:Immunoenzyme Techniques; D017403:In Situ Hybridization; D007371:Interferon-gamma / Q000235:genetics / Q000378:metabolism; D020382:Interleukin-18 / Q000235:genetics / Q000378:metabolism*; D015848:Interleukin-5 / Q000235:genetics / Q000378:metabolism; D008070:Lipopolysaccharides / Q000494:pharmacology; D008168:Lung / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D008875:Middle Aged; D010047:Ovalbumin / Q000494:pharmacology; D012333:RNA, Messenger / Q000378:metabolism; D012260:Ribonucleases; D017565:Sarcoidosis, Pulmonary / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D018417:Th1 Cells / Q000187:drug effects / Q000378:metabolism; D018418:Th2 Cells / Q000187:drug effects / Q000378:metabolism
chemical_list: D001798:Blood Proteins; D047091:Eosinophil Granule Proteins; D020382:Interleukin-18; D015848:Interleukin-5; D008070:Lipopolysaccharides; D012333:RNA, Messenger; D007371:Interferon-gamma; D010047:Ovalbumin; D012260:Ribonucleases