Individual cytokines contributing to asthma pathophysiology: valid targets for asthma therapy?
- PMID: 14758771
Individual cytokines contributing to asthma pathophysiology: valid targets for asthma therapy?
Abstract
Asthma is a common, chronic inflammatory condition of the airways that leads to airway hyperresponsiveness, reversible narrowing of the airways, and airway wall remodeling. Cytokines are involved in various aspects of asthma pathophysiology, such as the polarization of T-helper (Th)2 cells, antigen presentation, immunoglobulin (Ig)E response, airway wall remodeling, and mast cell and eosinophil recruitment and activation. Th2-derived cytokines, such as interleukin (IL)-4, IL-5 and IL-13 contribute to many of these aspects. Inhibition of individual cytokines for asthma therapy has been, and continues to be investigated. Anti-IL-5 monoclonal antibodies did not demonstrate beneficial effects in asthma, with only partial inhibition of eosinophilia in the airway wall; soluble IL-4 receptor, which neutralizes the effects of IL-4, has provided modest improvements in moderate asthma. The anti-IgE monoclonal antibody approach has demonstrated the most benefit in allergic asthma, particularly in severe disease. Which individual cytokine target can be inhibited with beneficial effects comparable to or above that of current inhaled corticosteroids can only be discovered through clinical trials. Blocking the effects of more than one cytokine may be more successful, and greater therapeutic effects may be observed in particular categories of asthma.
Similar articles
-
Agents against cytokine synthesis or receptors.Eur J Pharmacol. 2006 Mar 8;533(1-3):289-301. doi: 10.1016/j.ejphar.2005.12.046. Epub 2006 Feb 2. Eur J Pharmacol. 2006. PMID: 16457805 Review.
-
Effects of anticytokine therapy in a mouse model of chronic asthma.Am J Respir Crit Care Med. 2004 Nov 15;170(10):1043-8. doi: 10.1164/rccm.200405-681OC. Epub 2004 Aug 11. Am J Respir Crit Care Med. 2004. PMID: 15306533
-
4-1 BB stimulation inhibits allergen-specific immunoglobulin E production and airway hyper-reactivity but partially suppresses bronchial eosinophilic inflammation in a mouse asthma model.Clin Exp Allergy. 2006 Mar;36(3):377-85. doi: 10.1111/j.1365-2222.2006.02445.x. Clin Exp Allergy. 2006. PMID: 16499650
-
Anti-IL-13 monoclonal antibody inhibits airway hyperresponsiveness, inflammation and airway remodeling.Cytokine. 2004 Dec 21;28(6):224-32. doi: 10.1016/j.cyto.2004.08.007. Cytokine. 2004. PMID: 15566951
-
Regulatory T cells and asthma.Clin Exp Allergy. 2009 Sep;39(9):1314-23. doi: 10.1111/j.1365-2222.2009.03301.x. Epub 2009 Jun 17. Clin Exp Allergy. 2009. PMID: 19538496 Review.
Cited by
-
Steroid response in refractory asthmatics.Korean J Intern Med. 2012 Jun;27(2):143-8. doi: 10.3904/kjim.2012.27.2.143. Epub 2012 May 31. Korean J Intern Med. 2012. PMID: 22707883 Free PMC article. Review.