The interleukin‐33 receptor ST2 is important for the development of peripheral airway hyperresponsiveness and inflammation in a house dust mite mouse model of asthma

Several clinical and experimental studies have implicated IL‐33 and its receptor ST2 in the development of asthma. However, the effect of IL‐33/ST2 signalling on airway responses and inflammation in allergic asthma is not well established.

[1]  S. Dahlén,et al.  Interleukin‐33 exacerbates allergic bronchoconstriction in the mice via activation of mast cells , 2015, Allergy.

[2]  S. Akthar,et al.  Alternaria-derived serine protease activity drives IL-33–mediated asthma exacerbations , 2014, The Journal of allergy and clinical immunology.

[3]  Christopher S. Stevenson,et al.  Antigen-induced mast cell expansion and bronchoconstriction in a mouse model of asthma. , 2014, American journal of physiology. Lung cellular and molecular physiology.

[4]  S. Nakae,et al.  IL-33, but Not IL-25, Is Crucial for the Development of House Dust Mite Antigen-Induced Allergic Rhinitis , 2013, PloS one.

[5]  Cinzia L. Marchica,et al.  Allergen challenge during halothane compared to isoflurane anesthesia induces a more potent peripheral lung response , 2013, Respiratory Physiology & Neurobiology.

[6]  I. Sayers,et al.  IL-33 is more potent than IL-25 in provoking IL-13-producing nuocytes (type 2 innate lymphoid cells) and airway contraction. , 2013, The Journal of allergy and clinical immunology.

[7]  A. Bush,et al.  IL-33 promotes airway remodeling in pediatric patients with severe steroid-resistant asthma. , 2013, The Journal of allergy and clinical immunology.

[8]  G. Nilsson,et al.  Mast cell engraftment of the peripheral lung enhances airway hyperresponsiveness in a mouse asthma model. , 2012, American journal of physiology. Lung cellular and molecular physiology.

[9]  A. McKenzie,et al.  IL-33 citrine reporter mice reveal the temporal and spatial expression of IL-33 during allergic lung inflammation , 2012, European journal of immunology.

[10]  H. Hammad,et al.  Interleukin-1α controls allergic sensitization to inhaled house dust mite via the epithelial release of GM-CSF and IL-33 , 2012, The Journal of experimental medicine.

[11]  S. Wenzel.  Asthma phenotypes: the evolution from clinical to molecular approaches , 2012, Nature Medicine.

[12]  P. Mercier,et al.  Endogenous IL-33 Is Highly Expressed in Mouse Epithelial Barrier Tissues, Lymphoid Organs, Brain, Embryos, and Inflamed Tissues: In Situ Analysis Using a Novel Il-33–LacZ Gene Trap Reporter Strain , 2012, The Journal of Immunology.

[13]  M. Nawijn,et al.  The composition of house dust mite is critical for mucosal barrier dysfunction and allergic sensitisation , 2011, Thorax.

[14]  L. Gregory,et al.  Orchestrating house dust mite-associated allergy in the lung. , 2011, Trends in immunology.

[15]  Ryan D. Hernandez,et al.  Meta-analysis of Genome-wide Association Studies of Asthma In Ethnically Diverse North American Populations , 2011, Nature Genetics.

[16]  S. Nakae,et al.  IL-33 and Airway Inflammation , 2011, Allergy, asthma & immunology research.

[17]  D. Postma,et al.  Small airway disease in asthma and COPD: clinical implications. , 2011, Chest.

[18]  T. Abe,et al.  IL-33 is a crucial amplifier of innate rather than acquired immunity , 2010, Proceedings of the National Academy of Sciences.

[19]  Florence Demenais,et al.  A large-scale, consortium-based genomewide association study of asthma. , 2010, The New England journal of medicine.

[20]  G. Nilsson,et al.  Prostaglandin modulation of airway inflammation and hyperresponsiveness in mice sensitized without adjuvant. , 2010, Prostaglandins & other lipid mediators.

[21]  S. Dahlén,et al.  Comparison of Aerosol and Intranasal Challenge in a Mouse Model of Allergic Airway Inflammation and Hyperresponsiveness , 2010, International Archives of Allergy and Immunology.

[22]  Q. Hamid,et al.  Increased IL-33 expression by epithelial cells in bronchial asthma. , 2010, The Journal of allergy and clinical immunology.

[23]  I. McInnes,et al.  IL-33 Amplifies the Polarization of Alternatively Activated Macrophages That Contribute to Airway Inflammation1 , 2009, The Journal of Immunology.

[24]  Cinzia L. Marchica,et al.  Allergen-induced asthma in C57Bl/6 mice: Hyper-responsiveness, inflammation and remodelling , 2009, Respiratory Physiology & Neurobiology.

[25]  S. Toda,et al.  The mechanism of mucus production in bronchial asthma. , 2009, Current medicinal chemistry.

[26]  R. Hegde,et al.  Allergenicity resulting from functional mimicry of a Toll-like receptor complex protein , 2008, Nature.

[27]  K. Ulrich,et al.  Anti-inflammatory modulation of chronic airway inflammation in the murine house dust mite model. , 2008, Pulmonary pharmacology & therapeutics.

[28]  J. Fujimoto,et al.  Administration of IL-33 induces airway hyperresponsiveness and goblet cell hyperplasia in the lungs in the absence of adaptive immune system. , 2008, International immunology.

[29]  S. Holgate.  Epithelium dysfunction in asthma. , 2007, The Journal of allergy and clinical immunology.

[30]  P. Sly,et al.  Animal models of asthma , 2007, Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology.

[31]  J Fernando Bazan,et al.  IL-33, an interleukin-1-like cytokine that signals via the IL-1 receptor-related protein ST2 and induces T helper type 2-associated cytokines. , 2005, Immunity.

[32]  Jason H. T. Bates,et al.  The interface between measurement and modeling of peripheral lung mechanics , 2005, Respiratory Physiology & Neurobiology.

[33]  C. Taube,et al.  Strain‐specific differences in perivascular inflammation in lungs in two murine models of allergic airway inflammation , 2005, Clinical and experimental immunology.

[34]  D. Eidelman,et al.  IL-13 may mediate allergen-induced hyperresponsiveness independently of IL-5 or eotaxin by effects on airway smooth muscle. , 2005, American journal of physiology. Lung cellular and molecular physiology.

[35]  Jason H T Bates,et al.  The allergic mouse model of asthma: normal smooth muscle in an abnormal lung? , 2004, Journal of applied physiology.

[36]  P. Thompson,et al.  House Dust Mite Allergens Induce Proinflammatory Cytokines from Respiratory Epithelial Cells: The Cysteine Protease Allergen, Der p 1, Activates Protease-Activated Receptor (PAR)-2 and Inactivates PAR-11 , 2002, The Journal of Immunology.

[37]  D. J. Matthews,et al.  IL-9-deficient mice establish fundamental roles for IL-9 in pulmonary mastocytosis and goblet cell hyperplasia but not T cell development. , 2000, Immunity.

[38]  S. Galli,et al.  The diverse potential effector and immunoregulatory roles of mast cells in allergic disease. , 2000, The Journal of allergy and clinical immunology.

[39]  D. J. Matthews,et al.  T1/St2-Deficient Mice Demonstrate the Importance of T1/St2 in Developing Primary T Helper Cell Type 2 Responses , 2000, The Journal of experimental medicine.

[40]  C. Meisel,et al.  Crucial Role of the Interleukin 1 Receptor Family Member T1/St2 in T Helper Cell Type 2–Mediated Lung Mucosal Immune Responses , 1999, The Journal of experimental medicine.

[41]  I. Weeks,et al.  Magic Lite design and development. , 1989, Journal of bioluminescence and chemiluminescence.

[42]  Dirk E. Smith,et al.  Innate lymphoid cells responding to IL-33 mediate airway hyperreactivity independently of adaptive immunity. , 2012, The Journal of allergy and clinical immunology.

[43]  J. Bates,et al.  Dynamic mechanical consequences of deep inflation in mice depend on type and degree of lung injury. , 2004, Journal of applied physiology.

[44]  J. Bates,et al.  Measuring the lung function in the mouse: the challenge of size , 2003, Respiratory research.