Effect of Antagonists for NK2and B2Receptors on Antigen-induced Airway Responses in Allergic Rabbits

Woisin, F E; Matsumoto, Takayuki; Douglas, Garry J.; Paul, William; Whalley, Eric T.; Page, Clive

doi:10.1006/pupt.1999.0226

Cited by 13 publications

(2 citation statements)

References 49 publications

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“…Similar results were described by Perron [13] using another bradykinin B 1 receptor antagonist the LysLys [Hyp 3 , Igl 5 , Digl7, Oic 8 ] des-Arg 9 -bradykinin (code name B9858). Our results obtained with the bradykinin B 2 receptor antagonist (HOE-140) are in agreement with those of Woisin [21]. Using a rabbit model of allergic lung inflammation these authors found that pre-treatment with a potent and selective bradykinin B 2 receptor antagonist (D-Arg-Arg-Pro-HypGly-Thi-Ser-Dtic-NChg-Arg) (code name CP-0597), did not affect antigen-induced acute bronchoconstriction, airway hyperresponsiveness or pulmonary eosinophilia.…”

Section: Discussionsupporting

confidence: 92%

Modulation of allergic and immune complex-induced lung inflammation by bradykinin receptor antagonists

Landgraf

Jancar

Steil

et al. 2004

Inflammation Research

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Section: Discussionsupporting

confidence: 92%

Modulation of allergic and immune complex-induced lung inflammation by bradykinin receptor antagonists

Landgraf

Jancar

Steil

et al. 2004

Inflammation Research

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“…Nevertheless, the role of NK-1 and NK-2 receptors is often discussed controversially. To our present knowledge, blockade of NK-2 receptor may alter acute airway responses to antigen in animals but not antigen-induced lung eosinophilia [99]. According to recent results on guinea pigs, not only NK-2 but also NK-1 receptors might have important roles in the development of airway hyperresponsiveness [100].…”

Section: Classical Mediators As Targetsmentioning

confidence: 73%

Asthma therapy in the new millennium

Pahl¹,

Szelenyi²

2002

Inflamm. res.

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Bronchial asthma is one of the most common chronic diseases in modern society and yet, despite the availability of highly effective drugs, there is increasing evidence to suggest that its incidence is increasing. It is a general health problem in several industrialised countries and will remain one for the next decades. With regard to asthma pathogenesis, our understanding has increased tremendously over the last two decades. Therefore, the potential for specific targeted and constructed therapies has become evident. Monoclonal antibodies to IgE, soluble receptors or antibodies to certain cytokines such as IL-4 and IL-5 are being investigated as possible treatments for asthma. Besides the already known receptor antagonists, new compounds directed to novel receptor types (e.g. cytokine, adenosine, adhesion molecules, etc.) are now under development. New targets in the cytosol will come into focus. Preliminary studies of selective phosphodiesterase (PDE) inhibitors in asthmatic patients have been encouraging. It is also very likely that the use of glucocorticoids cannot be excluded from therapy. However, we should generate new glucocorticoids with less side-effects, probably by using the so-called retrometabolic drug design. The first representative of this new steroid class, loteprednol is already approved for the therapy of certain allergic disorders. Because asthma is a disease of many different gene polymorphisms, gene therapy seems to be of low success at present. Alternatively, antisense oligonucleotides could be used. Future developments may also include strategies targeting the remodeling of structural elements of the airways. Today's intensive search for new treatments should ensure a greater diversity of therapeutic possibilities for the management of asthma in the next millennium.

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