Are cytokines responsible for the asthmatic state of the airways?

Monaldi Arch Chest Dis. 1996 Jun;51(3):223-7.

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.

Publication types

  • Review

MeSH terms

  • Animals
  • Asthma / etiology*
  • Asthma / physiopathology
  • Cytokines / physiology*
  • Humans
  • Interleukin-1 / physiology
  • Interleukin-4 / physiology
  • Interleukin-5 / physiology
  • Tumor Necrosis Factor-alpha / physiology

Substances

  • Cytokines
  • Interleukin-1
  • Interleukin-5
  • Tumor Necrosis Factor-alpha
  • Interleukin-4