Are cytokines responsible for the asthmatic state of the airways?
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.
Kips
J C
JC
Dept of Respiratory Diseases, University Hospital Ghent, Belgium.
Pauwels
R A
RA
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
D016207:Cytokines; D007375:Interleukin-1; D015848:Interleukin-5; D014409:Tumor Necrosis Factor-alpha; D015847:Interleukin-4