Dihydropyridine Receptor Blockade in the Treatment of Asthma

Author(s): Lucette Pelletier, Jean-Charles Guery

Journal Name: Recent Patents on Inflammation & Allergy Drug Discovery
Continued as Recent Advances in Inflammation & Allergy Drug Discovery

Volume 2 , Issue 2 , 2008


Asthma is a chronic airway disease resulting from inappropriate Th2-cell biased activation. Interleukin (IL)-4, IL-5 and IL-13 produced by Th2 cells contribute to the inflammatory process. Attempts for inhibiting interleukin-4 or IL- 5 gave disappointing results. The simultaneous inhibition of several Th2-cytokines could be a more promising issue. Several arguments support the concept that Th2-cells express selective markers that could be targeted in asthma. Our group showed that Th2-cells selectively up-regulated dihydropyridine-sensitive Ca2+ (DHP-Ca) channels essential for Ca2+ signaling and type-2 cytokine production. Indeed, DHP-Ca antagonist effectively prevented or even reverted airway inflammation, airway remodeling and airway hyperresponsiveness in experimental models of asthma. Although it remains to be formally demonstrated that human lung infiltrating T-lymphocytes in asthmatic patients express DHP- Ca2+ channels, we hypothesize that targeting DHP-Ca channels in T-lymphocytes could represent an efficient strategy in the treatment of asthma.This review article also discussed patents relevant to the field.

Keywords: Asthma, dihydropyridine receptors or dihydropyridine-sensitive Ca2+ channels, airway hyperresponsiveness, calcium signaling, Th2-lymphocytes, interleukins 4, 5 and 13

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Article Details

Year: 2008
Published on: 01 March, 2012
Page: [109 - 116]
Pages: 8
DOI: 10.2174/187221308784543638
Price: $65

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