Interleukin‐4 and ‐13 expression is co‐localized to mast cells within the airway smooth muscle in asthma

Background Airway smooth muscle infiltration by mast cells is a feature of asthma and not eosinophilic bronchitis. In asthma, Th2 cytokines have been implicated as playing a critical role in the development of airway inflammation and hyper‐responsiveness. Whether inflammatory cells within the airway smooth muscle release these cytokines is unknown.

[1]  R. Panettieri,et al.  IL-13 and IL-4 promote TARC release in human airway smooth muscle cells: role of IL-4 receptor genotype. , 2003, American journal of physiology. Lung cellular and molecular physiology.

[2]  J. Stankova,et al.  CysLT1 receptor upregulation by TGF-beta and IL-13, but not IL-4, is associated with bronchial smooth muscle cell proliferation in response to LTD4 , 2003 .

[3]  A. Kay,et al.  The role of T lymphocytes in the pathogenesis of asthma. , 2003, The Journal of allergy and clinical immunology.

[4]  J. Stankova,et al.  CysLT1 receptor upregulation by TGF-beta and IL-13 is associated with bronchial smooth muscle cell proliferation in response to LTD4. , 2003, The Journal of allergy and clinical immunology.

[5]  I. Pavord,et al.  TH2 cytokine expression in bronchoalveolar lavage fluid T lymphocytes and bronchial submucosa is a feature of asthma and eosinophilic bronchitis. , 2002, The Journal of allergy and clinical immunology.

[6]  I. Pavord,et al.  Mast-cell infiltration of airway smooth muscle in asthma. , 2002, The New England journal of medicine.

[7]  S. Romagnani.  Cytokines and chemoattractants in allergic inflammation. , 2002, Molecular immunology.

[8]  Tak H. Lee,et al.  Selective induction of eotaxin release by interleukin-13 or interleukin-4 in human airway smooth muscle cells is synergistic with interleukin-1beta and is mediated by the interleukin-4 receptor alpha-chain. , 2002, American journal of respiratory and critical care medicine.

[9]  R. Panettieri,et al.  IL-13 and IL-4 cause eotaxin release in human airway smooth muscle cells: a role for ERK. , 2002, American journal of physiology. Lung cellular and molecular physiology.

[10]  R. Pauwels,et al.  The IL-5 receptor on human bronchus selectively primes for hyperresponsiveness. , 2002, The Journal of allergy and clinical immunology.

[11]  M. Grunstein,et al.  IL-13-dependent autocrine signaling mediates altered responsiveness of IgE-sensitized airway smooth muscle. , 2002, American journal of physiology. Lung cellular and molecular physiology.

[12]  A. Ammit,et al.  Human mast cell and airway smooth muscle cell interactions: implications for asthma. , 2001, American journal of physiology. Lung cellular and molecular physiology.

[13]  J. Kinet,et al.  Direct effects of interleukin-13 on signaling pathways for physiological responses in cultured human airway smooth muscle cells. , 2001, American Journal of Respiratory and Critical Care Medicine.

[14]  W. Busse,et al.  Efficacy of soluble IL-4 receptor for the treatment of adults with asthma. , 2001, The Journal of allergy and clinical immunology.

[15]  S. Holgate,et al.  The relative contribution of mast cell subsets to conjunctival TH2-like cytokines. , 2001, Investigative ophthalmology & visual science.

[16]  F. Annunziato,et al.  Expression of the Chemokine Receptor CCR3 on Human Mast Cells , 2001, International Archives of Allergy and Immunology.

[17]  J. Friend.  Do smoking parents seek the best advice for their asthmatic children? , 2001, Thorax.

[18]  A. Fraise,et al.  British Thoracic Society guidelines on diagnostic flexible bronchoscopy. , 2001, Thorax.

[19]  K. Chung,et al.  Effects of an interleukin-5 blocking monoclonal antibody on eosinophils, airway hyper-responsìveness, and the late asthmatic response , 2000, The Lancet.

[20]  Howarth,et al.  Localization of interleukin (IL) ‐4 but not IL‐5 to human mast cell secretory granules by immunoelectron microscopy , 2000, Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology.

[21]  I. Pavord,et al.  Induced sputum inflammatory mediator concentrations in eosinophilic bronchitis and asthma. , 2000, American journal of respiratory and critical care medicine.

[22]  A J Wardlaw,et al.  Eosinophils in asthma and other allergic diseases. , 2000, British medical bulletin.

[23]  L. Borish,et al.  Interleukin-4 receptor in moderate atopic asthma. A phase I/II randomized, placebo-controlled trial. , 1999, American journal of respiratory and critical care medicine.

[24]  F. Annunziato,et al.  Tryptase-chymase double-positive human mast cells express the eotaxin receptor CCR3 and are attracted by CCR3-binding chemokines. , 1999, The American journal of pathology.

[25]  A J Wardlaw,et al.  Eosinophilic bronchitis is an important cause of chronic cough. , 1999, American journal of respiratory and critical care medicine.

[26]  J. Black,et al.  Interleukin-4 inhibits mitogen-induced proliferation of human airway smooth muscle cells in culture. , 1998, American journal of physiology. Lung cellular and molecular physiology.

[27]  W. Sewell,et al.  Chronic cough resembles asthma with IL-5 and granulocyte-macrophage colony-stimulating factor gene expression in bronchoalveolar cells. , 1998, Journal of Allergy and Clinical Immunology.

[28]  I. Pavord,et al.  The use of induced sputum to investigate airway inflammation. , 1997, Thorax.

[29]  P. Howarth,et al.  Heterogeneity of human mast cells based on cytokine content. , 1995, Journal of immunology.

[30]  P. Howarth,et al.  Interleukin-4, -5, and -6 and tumor necrosis factor-alpha in normal and asthmatic airways: evidence for the human mast cell as a source of these cytokines. , 1994, American journal of respiratory cell and molecular biology.

[31]  P. Howarth,et al.  Immunohistochemistry on resin sections: a comparison of resin embedding techniques for small mucosal biopsies. , 1993, Biotechnic & histochemistry : official publication of the Biological Stain Commission.

[32]  J. Denburg,et al.  CHRONIC COUGH: EOSINOPHILIC BRONCHITIS WITHOUT ASTHMA , 1989, The Lancet.