Adenosine mediates IL-13–induced inflammation and remodeling in the lung and interacts in an IL-13–adenosine amplification pathway

Effects of IL-4 and IL-13 on adenosine receptor expression and responsiveness of the human mast cell line 1

“…In a study using IL-13 transgenic mice, IL-13 caused striking changes in adenosine receptor mRNA expression of the lung, the A 2A receptor expression being unaltered or decreased and A 1 , A 2B , and A 3 receptors being increased in their expression [31]. These results clearly suggest a relation between IL-13 and adenosine receptor expression, but as for IL-4, expression sites of the receptors were not investigated.…”

Adenosine: an endogenous regulator of innate immunity

“…However, the proinflammatory effects of mast-cell adenosine receptor stimulation, especially in situations associated with long-lasting high adenosine concentrations, seem to overshadowed the anti-inflammatory potential. Recent studies have revealed that mice, which accumulate high levels of endogenous adenosine owing to a deficiency of the adenosine catabolizing enzyme, adenosine deaminase, develop a pulmonary phenotype with mast cell-mediated inflammation resembling the symptoms of asthma [50][51][52]. This evidence, together with the observation that patients suffering from asthma have elevated pulmonary adenosine levels as well as augmented expression of adenosine receptors, suggests that increased adenosine signaling could be an important feature of asthma and chronic obstructive pulmonary diseases [53].…”

Airway remodeling contributes to the progressive loss of lung function in asthma: An overview

“…A partial list of various asthma inflammatory mediators is presented in Table II. 18,29,[37][38][39][40][41][42][43][44] There is no doubt, on the basis of in vivo studies, including airway challenge models, that airway inflammation is strongly associated with symptoms. Moreover, treatment that reduces inflammation effectively reduces morbidity and can reverse some aspects of remodeling.…”