A₃ receptors mediate rapid inflammatory cell influx into the lungs of sensitized guinea‐pigs

Abstract

5'-AMP caused a rapid migration of eosinophils and macrophages into the airways only in sensitized guinea-pigs, and this was blocked by the A3 antagonist MRS-1220. This was not associated with bronchial hyper-reactivity to histamine.

Role of adenosine receptors in regulating chemotaxis and cytokine production of plasmacytoid dendritic cells

“…[32][33][34] In a standard Transwell chemotaxis assay, we found that freshly isolated PDCs migrate toward gradients of adenosine in a concentration-dependent manner ( Figure 3A). Migration to adenosine was observed at physiologically relevant concentrations of 0.1 to 1.0 M, with maximal migration between 1.0 and 10 M (7.5% to 14.5% of total PDCs).…”

“…28,29 This ubiquitous molecule is used in selective signaling, activating membrane-bound adenosine receptors, denoted A 1 , A 2a , A 2b , and A 3 , which are widely distributed in tissues and mediate diverse biologic effects. 30,31 Adenosine has been recognized as an important modulator of immune responses, mediating inflammatory as well as anti-inflammatory effects, such as chemotaxis, [32][33][34] release of allergic mediators, 35 reduction of toxic oxygen metabolites, 36 neutrophil adherence to endothelium, 37 inhibition of T-cell activation, 38 and inhibition of cytokine production. [39][40][41][42][43][44] The nonredundant role of adenosine receptors in the regulation of inflammation in vivo has been demonstrated in A 2a receptor-deficient mice.…”

Involvement of Mast Cells in Adenosine-Mediated Bronchoconstriction and Inflammation in an Allergic Mouse Model

“…Previous studies from this laboratory have demonstrated that inhalation of adenosine causes a dose-related bronchoconstriction and the recruitment of inflammatory cells to the lung (Fan and Mustafa, 2002). Many other studies have also demonstrated that the acute inflammatory component of asthma can be characterized by the recruitment of eosinophils to the lungs (Spruntulis and Broadley, 2001). This recruitment of eosinophils to the lungs has been postulated to be the result of mast cell degranulation.…”

Identification of A3 Receptor- and Mast Cell-Dependent and -Independent Components of Adenosine-Mediated Airway Responsiveness in Mice

“…Moreover, airway responsiveness to adenosine has been shown to reflect the degree of underlying airway inflammation in a more sensitive fashion than does responsiveness to other agents that can induce nonspecific airway hyperreactivity in subjects with asthma, such as methacholine (10). In addition to its capacity to produce bronchoconstriction, adenosine has been shown to amplify the inflammatory response in some animal models of asthma following sensitization and challenge (11,12). In genetically engineered mice with elevated levels of adenosine due to adenosine deaminase (ADA) 3 deficiency, eosinophilic lung inflammation and mucus hypersecretion develop, and these animals die from respiratory failure at 3 wk of age (13).…”