John W. Bloom,
Professor of Pharmacology and Respiratory Sciences, M.D., Jefferson University, 1971
jbloom@resp-sci.arizona.edu

Molecular mechanisms of glucocorticoid action in the lung; mechanisms of eosinophil apoptosis; effects of genetic polymorphisms on gene expression in asthma.

My research is focused on the pathophysiology and drug therapy of asthma.  Current work in the laboratory is directed toward understanding the anti-inflammatory mechanisms of glucocorticoids. Glucocorticoids are the most effective therapy for asthma presently available, and inhaled glucocorticoids are being used as firstline therapy for asthma by many physicians. Glucocorticoid effects are mediated through glucocorticoid receptors which are ligand activated transcription factors. Studies are directed at determining the transcriptional mechanisms through which glucocorticoid receptors interact with other transcription factors to inhibit expression of inflammatory cytokine genes.  The overall goal of this research is to better understand the inflammatory mechanisms in asthma and develop more effective drug therapy.

Publications (Query PubMed for this investigator)

LeVan TD, Babin EA, Yamamura HI, and Bloom JW:  Pharmacological characterization of glucocorticoid receptors in primary human bronchial epithelial cells. Biochem Pharmacol, 57:1003-1009, 1999.

Bloom, JW: New insights into the molecular basis of glucocorticoid action. Immunology and Allergy Clinics of North America. 19: 653-670, 1999.

LeVan TD, Bloom JW, Adams DG, Hensel JL, and Halonen M:  Platelet-activating  factor induction of AP-1 signaling in bronchial epithelial cells.  Mol Pharmacol, 53:135-140, 1998.

Adkins KK, LeVan TD, Miesfeld RL, and Bloom JW:  GM-CSF regulation by glucocorticoids in bronchial epithelial cells: evidence for transcriptional mechanisms.  Am J Physiol, 19:L372-L378, 1998.

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