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Open Access Research article

Tachykinin receptors antagonism for asthma: a systematic review

Renata Ramalho15*, Raquel Soares2, Nuno Couto4 and André Moreira13

Author Affiliations

1 Department of Immunology, Faculty of Medicine, University of Porto, Porto, Portugal

2 Department of Biochemistry, Faculty of Medicine, University of Porto, Porto, Portugal

3 Department of Immunoallergology, Hospital of São João E.P.E., Porto, Portugal

4 Portuguese Oncology Institute IPOPFG-E.P.E, Porto, Portugal

5 Centro de Dermatologia Epidermis, Instituto CUF, Porto, Portugal

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BMC Pulmonary Medicine 2011, 11:41  doi:10.1186/1471-2466-11-41

Published: 2 August 2011

Abstract

Background

Tachykinins substance P, neurokinin A and neurokinin B seem to account for asthma pathophysiology by mediating neurogenic inflammation and several aspects of lung mechanics. These neuropeptides act mainly by their receptors NK1, NK2 and NK3, respectively which may be targets for new asthma therapy.

Methods

This review systematically examines randomized controlled trials evaluating the effect of tachykinins receptors antagonism on asthma. Symptoms, airway inflammation, lung function and airway inflammation were considered as outcomes. We searched the Cochrane Airways Group Specialized Register of Asthma Trials, Cochrane Database of Systematic Reviews, MEDLINE/PubMed and EMBASE. The search is as current as June 2010. Quality rating of included studies followed the Cochrane Collaboration and GRADE Profiler approaches. However, data were not pooled together due to different measures among the studies.

Results

Our systematic review showed the potential of NK receptor antagonist to decrease airway responsiveness and to improve lung function. However, effects on airway inflammation and asthma symptoms were poorly or not described.

Conclusion

The limited available evidence suggests that tachykinin receptors antagonists may decrease airway responsiveness and improve lung function in patients with asthma. Further large randomized trials are still required.