作者: Teal S. Hallstrand , Prescott G. Woodruff , Stephen T. Holgate , Darryl A. Knight
DOI: 10.1155/2012/160586
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摘要: An increasingly strong body of evidence implicates the airway epithelium as a critical regulator inflammation and remodeling relevant to pathogenesis asthma. The implicating includes in vivo studies humans murine models well vitro conducted with primary epithelial cells. purpose this special issue is provide forum integrate new knowledge about nature dysfunction asthma examine role immune function. articles contained within expound upon human examining gene expression, alterations structure, investigating function This contains 3 original research 4 review including some that delineate larger bodies work by well-established labs. focus on mechanisms related response fungal allergens, apoptosis, production mediators involved matrix, important injury IL-25 induction phase Two highlight pathways activation leading diverges from traditional Th2 paradigm. In final article, authors utility models. In paper entitled “Mechanisms asthmatic airways,” A. Shifren et al. group at Washington University Dr. Mario Castro others present an overview structural changes occur patients are particularly prominent severe particular, their outlines several these subepithelial matrix mucous cell further airflow obstruction. roles various therapies may target discussed. In “Apoptosis epithelium,” S. R. White Chicago presents thorough apoptosis health disease states focusing asthma, but also extending other pulmonary diseases. article has outstanding contrast cells basic regulate epithelium. clearly delineates have been identified animal reasons play pathogenic lung diseases involving epithelium. In “Responses environmental injury: childhood asthma,” K. Kumar New South Wales along P. Foster Newcastle detailed picture factors initiate inflammation. viral infection pollutants such diesel exhaust particles presented common triggers generation interleukin 25 (IL-25) thymic stromal lymphopoietin (TSLP). own using model systems studies. The “Immunopathology immunogenetics allergic bronchopulmonary aspergillosis,” was written Knutsen Department Pediatrics Saint Louis University. focuses aspergillosis (ABPA), characterized hypersensitivity associated central bronchiectasis markedly elevated IgE. By relating significant aspergillus mold antigens, author compelling plays key ABPA regulating lymphocyte trafficking activation. In titled, “Immunolocalization NLRP3 inflammasome normal following ovalbumin-induced inflammation,” H. B. Tran Adelaide use Little known aspect innate system or epithelium, found active caspase-1 redistribution caspase-1, IL-1β, IL 18 towards luminal surface sensitization challenge ovalbumin. These intriguing results should spur more into lead specific asthma. In “IL-17F induces CCL20 bronchial cells,” Nozato regulation expression IL-17F demonstrate modulates through mitogen-activated protein kinase (MAPK) pathway cyclic AMP element-binding (CREB) transcription factor. This adds investigative team demonstrating CXC chemokines, GM-CSF, IP-10, IL-11, IGF-1 pathway. In “Evaluation differentiated culture for research,” C. F. Stewart Nottingham working I. Sayers evaluated differences between investigators used lines adenocarcinoma line (Calu-3) SV-40-transformed (BEAS-2B). Using they there were markers differentiation cultured cells, junction proteins. Although basis know detail, donor cultures originated same raising questions variability systems. Taken together, yet takes center stage orchestrating responses inhaled environment influencing aberrant repair. addition, provides platform identifying novel therapeutic targets linked increasing resistance airways injury. We exceedingly grateful many leaders field biology who contributed issue. call papers well-recognized researchers additional emerging importance understanding asthma. Teal Hallstrand Prescott G. Woodruff Stephen T. Holgate Darryl Knight