title: Proinflammatory cytokines in allergic rhinitis.
abstract: Allergic diseases such as allergen-induced rhinitis represent an inflammatory reaction that is characterized by the chemotaxis and activation of various cell populations. A high degree of cell-to-cell communication is needed to orchestrate this inflammatory immune response. A variety of cytokines and adhesion receptors seem to play an important role in the allergic late phase reaction. Here we demonstrate that proinflammatory cytokines such as interleukin(IL)-1, IL-8 and TNF-alpha (tumor necrosis factor-alpha) can be detected in nasal secretions and mucosa by enzyme-linked immunosorbent assay and immunohistochemistry. The increased expression of adhesion receptors in mucosa specimens of patients with seasonal allergic rhinitis points to their role in regulating the cellular migration and probably represents a key event in allergic inflammation. We established an in vitro model using freshly taken nasal mucosa to study the induction of adhesion receptors by proinflammatory cytokines. E-selectin, an endothelial receptor, was strongly upregulated by IL-1 beta, TNF-alpha and allergen. The induction due to allergen exposure of the mucosa was markedly inhibited by soluble cytokine receptors (sIL-1R, TNF-BP) or by a receptor antagonist (IL-1ra) and prednisolone, These findings indicate that proinflammatory cytokines may be key factors for the upregulation of adhesion processes in human nasal mucosa and the activation of various cell populations involved in the allergic inflammation. They therefore represent a main target for new therapeutic strategies.
authors.affiliation: ENT Department, University of Düsseldorf, Germany.
authors.forename: C
authors.initials: C
authors.lastname: Bachert
authors.forename: U
authors.initials: U
authors.lastname: Hauser
authors.forename: B
authors.initials: B
authors.lastname: Prem
authors.forename: C
authors.initials: C
authors.lastname: Rudack
authors.forename: U
authors.initials: U
authors.lastname: Ganzer
mesh_terms: D015815:Cell Adhesion Molecules / Q000378:metabolism; D002450:Cell Communication / Q000276:immunology; D002633:Chemotaxis / Q000276:immunology; D019040:E-Selectin; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism; D007375:Interleukin-1 / Q000378:metabolism*; D016209:Interleukin-8 / Q000378:metabolism*; D016169:Lymphocyte Function-Associated Antigen-1 / Q000378:metabolism; D008562:Membrane Glycoproteins / Q000378:metabolism; D009297:Nasal Mucosa / Q000276:immunology / Q000378:metabolism; D011971:Receptors, Immunologic / Q000378:metabolism; D012130:Respiratory Hypersensitivity / Q000276:immunology* / Q000503:physiopathology; D012220:Rhinitis / Q000276:immunology* / Q000503:physiopathology; D006255:Rhinitis, Allergic, Seasonal / Q000276:immunology / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism*; D019010:Vascular Cell Adhesion Molecule-1
chemical_list: D015815:Cell Adhesion Molecules; D019040:E-Selectin; D007375:Interleukin-1; D016209:Interleukin-8; D016169:Lymphocyte Function-Associated Antigen-1; D008562:Membrane Glycoproteins; D011971:Receptors, Immunologic; D014409:Tumor Necrosis Factor-alpha; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1