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      Th2 cytokines and asthma — The role of interleukin-5 in allergic eosinophilic disease

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          Abstract

          Interleukin-5 is produced by a number of cell types, and is responsible for the maturation and release of eosinophils in the bone marrow. In humans, interleukin-5 is a very selective cytokine as a result of the restricted expression of the interleukin-5 receptor on eosinophils and basophils. Eosinophils are a prominent feature in the pulmonary inflammation that is associated with allergic airway diseases, suggesting that inhibition of interleukin-5 is a viable treatment. The present review addresses the data that relate interleukin-5 to pulmonary inflammation and function in animal models, and the use of neutralizing anti-interleukin-5 monoclonal antibodies for the treatment of asthma in humans.

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          Jak-STAT pathways and transcriptional activation in response to IFNs and other extracellular signaling proteins.

          Shona Kerr, I Kerr, G Stark … (1994)
          Through the study of transcriptional activation in response to interferon alpha (IFN-alpha) and interferon gamma (IFN-gamma), a previously unrecognized direct signal transduction pathway to the nucleus has been uncovered: IFN-receptor interaction at the cell surface leads to the activation of kinases of the Jak family that then phosphorylate substrate proteins called STATs (signal transducers and activators of transcription). The phosphorylated STAT proteins move to the nucleus, bind specific DNA elements, and direct transcription. Recognition of the molecules involved in the IFN-alpha and IFN-gamma pathway has led to discoveries that a number of STAT family members exist and that other polypeptide ligands also use the Jak-STAT molecules in signal transduction.
          Article 0 comments Cited 454 times – based on 0 reviews     Review now
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            Predominant TH2-like bronchoalveolar T-lymphocyte population in atopic asthma.

            D S Robinson, Q Hamid, S. Ying … (1992)
            In atopic asthma, activated T helper lymphocytes are present in bronchial-biopsy specimens and bronchoalveolar-lavage (BAL) fluid, and their production of cytokines may be important in the pathogenesis of this disorder. Different patterns of cytokine release are characteristic of certain subgroups of T helper cells, termed TH1 and TH2, the former mediating delayed-type hypersensitivity and the latter mediating IgE synthesis and eosinophilia. The pattern of cytokine production in atopic asthma is unknown. We assessed cells obtained by BAL in subjects with mild atopic asthma and in normal control subjects for the expression of messenger RNA (mRNA) for interleukin-2, 3, 4, and 5, granulocyte-macrophage colony-stimulating factor (GM-CSF), and interferon gamma by in situ hybridization with 32P-labeled complementary RNA. Localization of mRNA to BAL T cells was assessed by simultaneous in situ hybridization and immunofluorescence and by in situ hybridization after immunomagnetic enrichment or depletion of T cells. As compared with the control subjects, the subjects with asthma had more BAL cells per 1000 cell that were positive for mRNA for interleukin-2 (P less than 0.05), 3 (P less than 0.01), 4 (P less than 0.001), and 5 (P less than 0.001) and GM-CSF (P less than 0.001). There was no significant difference between the two groups in the number of cells expressing mRNA for interferon gamma. In the subjects with asthma, mRNA for interleukin-4 and 5 was expressed predominantly by T lymphocytes. Atopic asthma is associated with activation in the bronchi of the interleukin-3, 4, and 5 and GM-CSF gene cluster, a pattern compatible with predominant activation of the TH2-like T-cell population.
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              Interleukin 5 deficiency abolishes eosinophilia, airways hyperreactivity, and lung damage in a mouse asthma model

              IG Young, AJ Ramsay, KI Matthaei … (1996)
              Airways inflammation is thought to play a central role in the pathogenesis of asthma. However, the precise role that individual inflammatory cells and mediators play in the development of airways hyperreactivity and the morphological changes of the lung during allergic pulmonary inflammation is unknown. In this investigation we have used a mouse model of allergic pulmonary inflammation and interleukin (IL) 5-deficient mice to establish the essential role of this cytokine and eosinophils in the initiation of aeroallergen-induced lung damage and the development of airways hyperreactivity. Sensitization and aerosol challenge of mice with ovalbumin results in airways eosinophilia and extensive lung damage analogous to that seen in asthma. Aeroallergen-challenged mice also display airways hyperreactivity to beta-methacholine. In IL-5-deficient mice, the eosinophilia, lung damage, and airways hyperreactivity normally resulting from aeroallergen challenge were abolished. Reconstitution of IL-5 production with recombinant vaccinia viruses engineered to express this factor completely restored aeroallergen-induced eosinophilia and airways dysfunction. These results indicate that IL-5 and eosinophils are central mediators in the pathogenesis of allergic lung disease.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Respir Res
                Title: Respiratory Research
                Publisher: BioMed Central
                ISSN (Print): 1465-9921
                ISSN (Electronic): 1465-993X
                Publication date (Print): 2001
                Publication date (Electronic): 8 March 2001
                Volume: 2
                Issue: 2
                Pages: 71-79
                Affiliations
                [1 ]Allergy Department, Schering Plough Research Institute, Kenilworth, New Jersey, USA
                Article
                Publisher ID: rr41
                DOI: 10.1186/rr41
                PMC ID: 59571
                PubMed ID: 11686868
                SO-VID: dcaa27d6-9d60-4554-934a-330fe8ee8695
                Copyright © Copyright © 2001 BioMed Central Ltd
                History
                Date received : 22 December 2000
                Date revision requested : 29 January 2001
                Date revision received : 16 February 2001
                Date accepted : 19 February 2001
                Categories
                Subject: Review

                ScienceOpen disciplines: Respiratory medicine
                Keywords: allergy,eosinophil,asthma,interleukin-5
                Data availability:
                ScienceOpen disciplines: Respiratory medicine
                Keywords: allergy, eosinophil, asthma, interleukin-5

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