Michael R. Blackburn

TL;DR: It is demonstrated that the A(1)AR plays an anti-inflammatory and/or protective role in the pulmonary phenotype seen in ADA-deficient mice, which suggests that A( 1)AR signaling may serve to regulate the severity of pulmonary inflammation and remodeling seen in chronic lung diseases by controlling the levels of important mediators of pulmonaryinflammation and damage.

TL;DR: Investigation of adenosine receptor-dependent regulation of interleukin (IL)-6 and TNF-α blood plasma levels in A2BKO and wild-type mice in vivo and their release from peritoneal macrophages ex vivo indicates that stimulation of A 2B receptors up-regulates the proinflammatory cytokine IL-6 and argues against the recently suggested anti-inflammatory role of A1B receptors.

TL;DR: S sustained adenosine exposure may cause mitochondrial oxidative stress, leading to activation of p38, JNK, and RhoA in mitochondria and resulting in EC barrier dysfunction, which is critical to the maintenance of the alveolar-capillary barrier.

TL;DR: A novel mechanism of disease progression to pulmonary hypertension is identified and the development of A2BR antagonists for the treatment of pulmonary hypertension secondary to interstitial lung disease is supported.