Robert J. Homer, M.D., Ph.D.



Professor of Pathology and Internal Medicine (Pulmonary);
Director, Medical Student Course Module.

Department of Pathology
Yale University School of Medicine
P.O. Box 208023
310 Cedar Street LH 108
New Haven, CT 06520-8023

Office: VA: 203-932-5711 x3319
Lab: 203-785-2788
Fax: 203-785-7303

email: robert.homer@yale.edu


Training:
Post-doctoral fellowship (Molecular Immunology),Yale University, New Haven, CT, 1989-91
Residency (Pathology), Yale New Haven Hospital, 1987-92
Ph.D. (Immunology), Yale University, New Haven, CT, 1987
M.D., Yale Univ. School of Medicine, 1987
B.A. (Physics), Harvard College, Cambridge, MA, 1979

Expertise:
lung pathology; interstitial lung disease: immunopathology; pathology of animal models of asthma, pulmonary fibrosis, acute lung injury, emphysema.

Research Interests:
(1) Pathology of asthma and other inflammatory lung diseases. I am the director of the morphology core of an NIH-funded asthma SCOR (specialized center for research) as well as the pathology co-principle investigator on several other NIH grants relating to inflammatory lung disease including emphysema. As such I select, perform, and analyze appropriate morphologic assays, primarily for light microscopy, but also for electron microscopy. Models under analysis include mice transgenic for various cytokines (IL-6 family, IL-13, IL-10), mice deficient in various cytokines or their receptors (IL-4, Stat-6, CCR2) or other mediators (MMP-9, NF-kappa B) and various adoptive transfer models. These mice are also subject to other stresses, especially hyperoxia. Some human work on isocyanate induced asthma is also ongoing. 2) Miscellaneous interests include autopsy pathology, case reports, and quality assurance issues in pathology.

interstitial lung disease, asthma, emphysema, pulmonary fibrosis, animal models of lung disease

Professional Service:
Besides signout and administrative responsibilities at the West Haven VA, I am also responsible for the research histology laboratory at Yale, a shared facility of the Yale Comprehensive Cancer Center and a component of the Department of Pathology's Program in Critical Technologies

Other Links:

Surgical Pathology
VA Connecticut
Critical Technologies
Community of Science (COS) Database

Selected Publications:

Cohn, L., Homer, R. J., Marinov, A., Rankin, J. and Bottomly, K. 1997. Induction of airway mucus production By T helper 2 (Th2) cells: a critical role for interleukin 4 in cell recruitment but not mucus production. J Exp Med 186:1737-47.

Trawick, D., Kotch, A., Matthay, R. and Homer, R. J. 1997. Eosinophilic pneumonia as a presentation of occult chronic granulomatous disease. Eur Respir J 10:2166-70.

Waxman, A. B., Einarsson, O., Seres, T., Knickelbein, R. G., Warshaw, J. B., Johnston, R., Homer, R. J. and Elias, J. A. 1998. Targeted lung expression of interleukin-11 enhances murine tolerance of 100% oxygen and diminishes hyperoxia-induced DNA fragmentation. J Clin Invest 101:1970-82.

Zhu, Z., Homer, R. J., Wang, Z., Chen, Q., Geba, G. P., Wang, J., Zhang, Y. and Elias, J. A. 1999. Pulmonary expression of interleukin-13 causes inflammation, mucus hypersecretion, subepithelial fibrosis, physiologic abnormalities, and eotaxin production. J Clin Invest 103:779-88.

Zheng, T., Zhu, Z., Wang, Z., Homer, R. J., Ma, B., Riese, R. J., Jr., Chapman, H. A., Jr., Shapiro, S. D. and Elias, J. A. 2000. Inducible targeting of IL-13 to the adult lung causes matrix metalloproteinase- and cathepsin-dependent emphysema. J Clin Invest 106:1081-93.

Elias, J. A., Zhu, Z., Chupp, G. and Homer, R. J. 1999. Airway remodeling in asthma. J Clin Invest 104:1001-6.

Homer, R. J., Z. Zhu, L. Cohn, C. G. Lee, W. I. White, S. Chen, and J. A. Elias. Differential expression of chitinases identify subsets of murine airway epithelial cells in allergic inflammation. Am J Physiol Lung Cell Mol Physiol 2006;291:L502-11.

Kang, M. J., R. J. Homer, A. Gallo, C. G. Lee, K. A. Crothers, S. J. Cho, C. Rochester, H. Cain, G. Chupp, H.J. Yoon, and J. A. Elias. IL-18 Is Induced and IL-18 Receptor {alpha} Plays a Critical Role in the Pathogenesis of Cigarette Smoke-Induced Pulmonary Emphysema and Inflammation. J Immunol 2007;178:1948-1959.

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This page was last modified on: 11/16/2009