University of California San Francisco
San Francisco General Hospital
Box 0854, Bldg 1-150
San Francisco, California 94143
phone: (415) 206-6650
fax: (415) 206-4123
email: rvenk@itsa.ucsf.edu

Dr. Venkayya received his M.D. degree in 1991 from the 6-year combined B.S./M.D. program at the Northeastern Ohio Universities College of Medicine. He completed his residency at the University of Michigan in 1994, and remained there as a Chief Medical Resident from 1994-95. He then began his fellowship in Pulmonary & Critical Care Medicine at the University of California, San Francisco, where continued as a member of the faculty in 1999. Dr. Venkayya is based at San Francisco General Hospital, where he is the Co-Director of the Medical Intensive Care Unit and the Director of the High-Risk Asthma Clinic. He is a member of the Lung Biology Center, where he investigates mechanisms of airway hyperresponsiveness using a murine model of asthma.

Research Interests

I am interested in understanding the events that lead to the airway narrowing found in asthma. To investigate these processes, I use a modification of a murine model of asthma. Traditional allergic models of asthma require the sensitization of naïve mice with antigens such as ovalbumin or Aspergillus culture extract. These protocols induce significant eosinophil-rich airway inflammation that is associated with airway hyperresponsiveness (AHR), which is a hallmark of the human disease of asthma. The complexity of airway inflammation found in these models, however, makes it difficult to identify specific pathways that lead to AHR.

Lymphocytes have been shown to be critically important for the development of AHR in these models. Understanding this, we have worked to identify specific lymphocyte mediators that might act directly upon resident airway cells such as epithelial cells or smooth muscle cells to induce AHR. Our investigations began with the finding that Th2 lymphocyte-conditioned medium could rapidly induce AHR when administered to the airways of naïve mice, in the absence of significant airway inflammation. More recently, we have confirmed that the cytokines IL-4 and IL-13 are required for this effect. Our current investigations are focused on the downstream events that result in AHR.

I have maintained a significant interest in clinical medicine, and research questions that can only be answered by clinical research. I began the High-Risk Asthma Clinic at SFGH, in order to address the needs of this population and to identify a population for future clinical investigation.

Recent Publications

1. Venkayya R, Lam M, Willkom M, Grunig G, Corry DB, Erle DJ.  “The Th2 Lymphocyte Products IL-4 and IL-13 Rapidly Induce Airway Hyperresponsiveness Through Direct Effects on Resident Airway Cells.” (Am J Resp Cell Mol Bio, in press).

2. Ford JG, Rennick D, Donaldson DD, Venkayya R, McArthur C, Hansell E, Kurup VA, Warnock M, Grunig G.  IL-13 and IFNg - interactions in lung inflammation.  Journal of Immunology 2001:167: 1769-1777

3. Grünig G, Warnock M, Wakil AE, Venkayya R, Brombacher F, Rennick DM, Sheppard D, Mohrs M, Donaldson DD, Locksley RM, Corry DB. "Requirement for IL-13 Independently of IL-4 in Experimental Asthma." Science 1998:282;2261-63.

4. Venkayya R, Corry DB, Wagner N, Mueller W, Erle DJ. 1998. The integrin b7 is necessary for development of airway hyperresponsiveness, but not airway inflammation, in a murine model of asthma.. Am J Respir Crit Care Med 157(3):A244 (Abstract).