The "Asthma Clinical Core B" will be a resource to provide well characterized subjects and specimens from cohorts of asthma and control subjects (bronchial brushings, BAL, endobronchial biopsy, sputum, blood, lung tissue) that will be used in each of the three projects comprising this AADCRC (Broide, Project 1;Croft, Project 2;Zuraw, Project 3). These specimens will allow investigators in the AADCRC to determine whether the inflammatory and remodeling pathways they are studying are differentially regulated in asthma compared to a control population. In addition to the cross sectional cohorts of asthma and control subjects. Core B will also provide specimens (sputum, blood, BAL, bronchial brushings, endobronchial biopsy) from well characterized asthmatic subjects obtained before and after allergen challenge, as well as before and after rhinoviral challenge. Overall, the provision of these specimens from asthma and control subjects will allow the individual projects to determine whether defined inflammatory and remodeling pathways are different in asthma compared to control subjects, as well as determine whether these inflammatory and remodeling pathways are regulated to be expressed by two common precipitants of asthma namely allergen and virus.
Inhalation of airborne allergens such as cat and dust mite or respiratory viruses may result in damage and scarring of the bronchial tubes in susceptible asthmatics. This project will provide increased understanding of the cause of this scarring and suggest potential ways to identify asthmatics at risk for developing scarring of their lungs, or potential new treatments.
|Das, Sudipta; Miller, Marina; Beppu, Andrew K et al. (2016) GSDMB induces an asthma phenotype characterized by increased airway responsiveness and remodeling without lung inflammation. Proc Natl Acad Sci U S A 113:13132-13137|
|Mehta, Amit K; Duan, Wei; Doerner, Astrid M et al. (2016) Rhinovirus infection interferes with induction of tolerance to aeroantigens through OX40 ligand, thymic stromal lymphopoietin, and IL-33. J Allergy Clin Immunol 137:278-88.e6|
|Rajan, Jessica; Newbury, Robert O; Anilkumar, Arjun et al. (2016) Long-term assessment of esophageal remodeling in patients with pediatric eosinophilic esophagitis treated with topical corticosteroids. J Allergy Clin Immunol 137:147-56.e8|
|Herro, Rana; Croft, Michael (2016) The control of tissue fibrosis by the inflammatory molecule LIGHT (TNF Superfamily member 14). Pharmacol Res 104:151-5|
|Zhou, Weisong; Toki, Shinji; Zhang, Jian et al. (2016) Prostaglandin I2 Signaling and Inhibition of Group 2 Innate Lymphoid Cell Responses. Am J Respir Crit Care Med 193:31-42|
|Mehta, Amit K; Gracias, Donald T; Croft, Michael (2016) TNF activity and T cells. Cytokine :|
|Rawson, Renee; Yang, Tom; Newbury, Robert O et al. (2016) TGF-Î²1-induced PAI-1 contributes to a profibrotic network in patients with eosinophilic esophagitis. J Allergy Clin Immunol 138:791-800.e4|
|Miller, Marina; Esnault, Stephane; Kurten, Richard C et al. (2016) Segmental allergen challenge increases levels of airway follistatin-like 1 in patients with asthma. J Allergy Clin Immunol 138:596-599.e4|
|Karta, Maya R; Broide, David H; Doherty, Taylor A (2016) Insights into Group 2 Innate Lymphoid Cells in Human Airway Disease. Curr Allergy Asthma Rep 16:8|
|Kim, Alexander S; Doherty, Taylor A; Karta, Maya R et al. (2016) Regulatory B cells and T follicular helper cells are reduced in allergic rhinitis. J Allergy Clin Immunol 138:1192-1195.e5|
Showing the most recent 10 out of 87 publications