title: Are cytokines responsible for the asthmatic state of the airways?
abstract: Chronic mucosal airway inflammation is currently considered to be the central element in the pathophysiology of asthma. This inflammatory process is regulated by a complex network of mutually interacting cytokines. The overall pattern of cytokine expression in asthma is one of increased expression of T-helper 2-like cytokines, including interleukin (IL)-4 and IL-5, in addition to proinflammatory cytokines, such as tumour necrosis factor-alpha (TNF-alpha) and IL-1 beta. The precise functional importance of each of these cytokines within the global network remains to be fully established. This question has been addressed in a number of in vivo animal studies. Combining these data with descriptive findings in man makes it possible to address somewhat further the question of the in vivo significance of a specific cytokine in the asthmatic state of the airways. This paper reviews some of the data currently available on this subject.
authors.affiliation: Dept of Respiratory Diseases, University Hospital Ghent, Belgium.
authors.forename: J C
authors.initials: JC
authors.lastname: Kips
authors.forename: R A
authors.initials: RA
authors.lastname: Pauwels
mesh_terms: D000818:Animals; D001249:Asthma / Q000209:etiology* / Q000503:physiopathology; D016207:Cytokines / Q000502:physiology*; D006801:Humans; D007375:Interleukin-1 / Q000502:physiology; D015847:Interleukin-4 / Q000502:physiology; D015848:Interleukin-5 / Q000502:physiology; D014409:Tumor Necrosis Factor-alpha / Q000502:physiology
chemical_list: D016207:Cytokines; D007375:Interleukin-1; D015848:Interleukin-5; D014409:Tumor Necrosis Factor-alpha; D015847:Interleukin-4