Dr. Hasday is Board-certified in Internal Medicine, Pulmonary Medicine and Critical Care Medicine and is Head of the Pulmonary and Critical Care Medicine Division. His areas of clinical expertise are acute lung injury, sepsis, and interstitial lung diseases.
Dr. Hasday is internationally recognized for work on the immunomodulatory effects of physiologically relevant changes in temperature. His bedside-to-bench-to-bedside research on the basic mechanisms through which febrile-range hyperthermia (FRH) modulates host defenses has produced a substantial body of work in this area in the last decade.He recently reported that FRH dramatically increases pulmonary oxygen therapy. This work spans the range from the basic molecular and cell biology to whole animal models and clinical trials. If confirmed in humans, this will lead to a practice-altering ARDS study to originate from the Division. Dr. Hasday and colleagues at the University of Maryland have advanced a concept that fever borrows some heat-shock mechanisms, including the central heat-shock-activated transcription factor, Heat Shock Factor-1 (HSF-1), which act in different ways at febrile and heat-shock temperatures. His studies in HSF-1 knockout mice showing that heat shock increases lung inflammation and injury may lead to new therapeutic modalities.
Dr. Hasday has also showed that clinically-relevant hypothermia prolongs expression of the proinflammatory cytokines TNF and IL-1ß in monocyte cultures and blocks apoptosis in epithelial cells. He has recently shown that this effect is even more global in that activation of the pivotal transcription factor, NFkappaB, is prolonged in hypothermic cell. Since NFkappaB activates both proinflammatory cytokine genes and anti-apoptosis genes, this exciting finding may explain both the cytoprotective effects of hypothermia as well as its association with higher circulating cytokine levels and inreased mortality in patients with sepsis.