title: Mechanisms of asthma.
abstract: Airway inflammation is a key factor in the mechanisms of asthma. Articles published in the Journal of Allergy and Clinical Immunology this past year have highlighted the utility of investigative bronchoscopy with segmental antigen challenge and induced sputum analyses to evaluate features of airway inflammation in relationship to asthma severity. Peripheral blood cell generation of cytokines IFN-gamma (T(H)1) and IL-5 (T(H)2) was used to evaluate the relationship of the balance of T(H)1/T(H)2 cytokines to asthma persistence and severity in a 42-year, longitudinal study. Chemokines, including thymus and activation-regulated chemokine, are important to the regulation of inflammation and IgE synthesis. Their potential role in asthma has also been evaluated. Finally, albuterol (R)- and (S)-enantiomers may have distinct effects on airway relaxation and regulation of inflammation, suggesting the possibility that monoisomeric therapy has therapeutic advantages. The potential contribution of genetic factors and mechanisms to airway inflammation and remodeling also continues to be an area of intense investigation. During the past year a number of articles published in the Journal of Allergy and Clinical Immunology have identified and clarified potential genetic mechanisms in asthma. The contribution of genetics to asthma has been examined in a wide variety of studies, ranging from epidemiologic association and twin studies all the way to molecular analysis through microarray gene expression experiments.
authors.affiliation: Allergy and Clinical Immunology, University of Wisconsin Department of Medicine, Madison, WI, USA.
authors.forename: William W
authors.initials: WW
authors.lastname: Busse
authors.forename: Lanny J
authors.initials: LJ
authors.lastname: Rosenwasser
mesh_terms: D000225:Adenine / Q000031:analogs & derivatives* / Q000627:therapeutic use; D000328:Adult; D000420:Albuterol / Q000627:therapeutic use; D001249:Asthma / Q000188:drug therapy / Q000235:genetics* / Q000276:immunology*; D001993:Bronchodilator Agents / Q000627:therapeutic use; D018925:Chemokines / Q000276:immunology; D002648:Child; D016207:Cytokines / Q000276:immunology; D018450:Disease Progression; D020022:Genetic Predisposition to Disease; D006801:Humans; D007073:Immunoglobulin E / Q000096:biosynthesis; D007249:Inflammation / Q000276:immunology; D007371:Interferon-gamma / Q000276:immunology; D015848:Interleukin-5 / Q000276:immunology
chemical_list: D001993:Bronchodilator Agents; D018925:Chemokines; D016207:Cytokines; D015848:Interleukin-5; C088989:N(6)-(1,3-dimethyl-2-butenyl)adenine; D007073:Immunoglobulin E; D007371:Interferon-gamma; D000225:Adenine; D000420:Albuterol