Thomas Jefferson University
Postdoctoral Fellow
Baylor College of Medicine

Areas of Interest

Research Interests

Purinergic signaling, regulation of lung disease

Research Information

Adenosine Signaling and Chronic Lung Disease

Inflammatory and remodeling responses are prominent features of chronic lung diseases such as asthma, chronic obstructive pulmonary disease (COPD), pulmonary fibrosis and pulmonary hypertension. Although signaling pathways associated with the genesis of inflammation and the control of tissue remodeling have been described, little is known about signaling pathways that serve to regulate the chronicity of these pulmonary disorders with the intent of developing novel therapeutic strategies.

A central hypothesis of my laboratory is that the signaling nucleoside adenosine is an amplifier of lung inflammation and damage. Adenosine is generated in response to cell damage and it is our belief that as adenosine levels increase in the lung they access pathways that serve to promote airway inflammation and remodeling. Adenosine signals by engaging specific adenosine receptors on target cells such as inflammatory cells, fibroblasts, airway epithelial cells and smooth muscle cells. Most of the projects in my laboratory focus on understanding the mechanisms by which adenosine receptor signaling influences the activities of these cells in the context of lung inflammation and remodeling.

We make extensive use of genetically modified mice to examine the role of adenosine signaling in chronic lung disease. This includes knockout mice of components of adenosine metabolism and signaling. We also conduct mechanistic experiments in disease relevant cell types and work extensively with human explanted lungs obtained following lung transplantation here in the Texas Medical Center. These translational approaches help us identify novel strategies for treating chronic lung disease.

Blackburn graphic

Working Model: We hypothesize that extracellular adenosine in response to numerous injuries
contributes to an abnormal wound healing response by engaging the adenosine A2B receptor (A2BR). We are currently investigating specific mechanisms of heightened adenosine signaling in disease
relevant cells and tissues. Our hope is to advance the use of adenosine-based therapeutics for the
treatment of chronic lung diseases.

Selected Publications

Luo F, Le NB, Mills T, Chen NY, Karmouty- Quintana H, Molina JG, Davies J, Philip K, Volcik KA, Liu H, Xia Y, Eltzschig HK, Blackburn MR. 2016. Extracellular adenosine levels are associated with the progression and exacerbation of pulmonary fibrosis. FASEB J. 30(2):874-83.

Weng T, Poth JM, Karmouty-Quintana H, Garcia-Morales LJ, Melicoff E, Luo F, Chen NY, Evans CM, Bunge RR, Bruckner BA, Loebe M, Volcik KA, Eltzschig HK, Blackburn MR. 2014. Hypoxia-induced deoxycytidine kinase contributes to epithelial proliferation in pulmonary fibrosis. Am J Respir Crit Care Med. 190(12):1402-12.

Karmouty-Quintana H, Philip K, Acero LF, Chen NY, Weng T, Molina JG, Luo F, Davies J, Le NB, Bunge I, Volcik KA, Le TT, Johnston RA, Xia Y, Eltzschig HK, Blackburn MR. 2015. Deletion of ADORA2B from myeloid cells dampens lung fibrosis and pulmonary hypertension. FASEB J. 29(1):50-60.