Bethany B. Moore, Ph.D.
Associate Professor,
Internal Medicine, Pulmonary Division

bmoore@umich.edu



Research Interests:

My laboratory has two basic areas of interest. Our primary focus involves
the pathogenesis of pulmonary fibrosis and the second interest involves
infectious complications of bone marrow transplantation. Pulmonary fibrosis
is a disease, often of unknown etiology, that results in the progressive
accumulation of extracellular matrix (collagen) deposition within the lung
resulting in a loss of gas exchange and death from respiratory insufficiency. The excessive collagen deposition that occurs in fibrosis is the result of activation and differentiation of fibroblasts into cells called myofibroblasts which contract the lung architecture. The combination of this contractile phenotype with the increased collagen synthetic capacity of these cells makes them the pathologic entity in this disease process. Many clinical associations suggest that viral infections may be associated with fibrotic illness.Thus, my laboratory is currently working to understand how viral infections impact the development of pulmonary fibrosis. We also study the contribution of a novel cell type, the fibrocyte, to pulmonary fibrogenesis.

The other area of interest in our laboratory involves studying bacterial and viral
infections following bone marrow transplantation (BMT).Patients who undergo BMT remain more susceptible to lung infections for years post-BMT. Thus, we developed an animal model to study this question. Following syngeneic BMT, mice are more susceptible to infection with the nosocomial pathogen Pseudomonas aeruginosa as well as to herpesviral infections despite bone marrow reconstitution. We have determined that this increased susceptibility to bacterial pathogens relates to increased production of prostaglandin E2 post-BMT. The increased PGE2 production impairs the phagocytic and killing ability of the donor-derived alveolar macrophages. In the setting of viral infection, we are exploring the role that transforming growth factor beta plays in the inhibition of anti-viral effector T cell responses.

Recent Publications:

Ballinger, MN, Aronoff, DM, McMillan, TR, Cooke, KR, Olkiewicz, K, Toews, GB, Peters-Golden, M and BB Moore. 2006. Critical Role of Prostaglandin E2 Overproduction in Impaired Pulmonary Host Response Following Bone Marrow Transplantation. J. Immunol. 177:5499-5508.

Ballinger, MN, McMillan, TR and BB Moore. 2007. Eicosanoid regulation of pulmonary innate immunity post-hematopoietic stem cell transplantation. Arch. Immunol. Ther. Exp.55:1-12.

Vannella, KM, McMillan, TR, Charbeneau, RP, Wilke, CA, Toews, GB, Peters-Golden, M, and BB Moore. 2007. Cysteinyl leukotrienes are autocrine and paracrine regulators of fibrocyte function. J. Immunol. 179(11)7883-90.

Moore, BB and C.M. Hogaboam, 2008. Murine Models of Pulmonary Fibrosis. Am. J. Physiol. Lung Cell Mol. Physiol. 294:L152-60.

McMillan,TR, Moore, BB, Weinberg, JB, Vannella, KM, Fields, WB, Christensen, PJ, van Dyk, LF and Towes, GB, 2008. Exacerbation of established pulmonary fibrosis in an animal model by gammaherpesvirus. Am. J. Respir. Crit. Care Med. 177(7):771-80.

Hubbard, LN Ballinger, MN, Wilke, CA and Moore, BB. 2008. Comparison of conditioning regimens for alveolar macrophage reconstitution and innate immune function post-Bone Marrow Transplantation. Exp. Lung Res. 34:263-275.

Ballinger, MN, Hubbard, LN, McMillan, TR, Toews, GB, Peters-Golden, M, Paine, R and BB Moore. 2008. Role of granulocyte macrophage colony stimulating factor in pulmonary host defense post-bone marrow transplantation. Am. J. Physiol. Lung Cell Mol. Physiol. 295(1):L114-22.

Vannella, KM and BB Moore. 2008. Viruses as Co-Factors in the Initiation or Exacerbation of Lung Fibrosis. Fibrogenesis and Tissue Repair 1:2.