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Effect of choline chloride in allergen-induced mouse model of airway inflammation

¹ Allergy and Immunology Section, Institute of Genomics and Integrative Biology, and, ³ Dept of Respiratory Medicine, Vallabhbhai Patel Chest Institute, University of Delhi, Delhi, and ² Dept of Biotechnology, University of Pune, Pune, India.

CORRESPONDENCE: B. P. Singh, Allergy and Immunology Section, Room No. 509, Institute of Genomics and Integrative Biology, Delhi University Campus, Mall Road, Delhi-110007, India. Fax: 91 1127667471. E-mail: singhbp1951{at}yahoo.com

Keywords: Airway inflammation, animal model, asthma, choline, eosinophils

Received: February 16, 2007
Accepted June 20, 2007

The incidence of asthma has increased the world over, and current therapies for the disease suffer from potential side-effects. This has created an opportunity to develop novel therapeutic approaches. Here, the anti-inflammatory activity of choline was investigated in a mouse model of allergic airway inflammation.

Choline (1 mg·kg^–1) was administered via oral gavage or intranasally before and after ovalbumin (OVA) challenge in sensitised mice. Airway hyperresponsiveness (AHR) to methacholine was measured in the mice by whole-body plethysmography. Type-2 T-helper cell cytokine and leukotriene levels were estimated in bronchoalveolar lavage fluid (BALF) and spleen culture supernatant by ELISA. Eosinophil peroxidase activity was also determined in the BALF supernatant.

Choline treatment in sensitised mice before OVA challenge via oral/intranasal routes significantly inhibited eosinophilic airway inflammation and eosinophil peroxidase activity. It also reduced immunoglobulin E and G1 production and inhibited the release of type-2 T-helper cell cytokines and leukotrienes. However, the development of AHR was prevented effectively by intranasal choline treatment. Most importantly, choline treatment after OVA challenge by both routes could reverse established asthmatic conditions in mice by inhibiting AHR, eosinophilic airway inflammation and other inflammatory parameters.

This study provides a new therapeutic approach for controlling as well as preventing asthma exacerbations.

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