Robert J Homer MD, PhD

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

Research Interests

Lung pathology; Interstitial lung disease; immunopathology; Pathology of animal models of asthma; Pulmonary fibrosis; Acute lung injury; Emphysema


Research Summary

(1) Pathology of asthma and other inflammatory lung diseases. I am the pathology co-principle investigator on several 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.

Extensive Research Description

(1) Pathology of asthma and other inflammatory lung diseases. I am the pathology co-principle investigator on several 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


Selected Publications

  • Homer, R. J., J. A. Elias, C. G. Lee, and E. Herzog. Modern concepts on the role of inflammation in pulmonary fibrosis. Arch Pathol Lab Med 2011;135:780-788.
  • 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.
  • 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.
  • Lee, C. G., S. J. Cho, M. J. Kang, S. P. Chapoval, P. J. Lee, P. W. Noble, T. Yehualaeshet, B. Lu, R. A. Flavell, J. Milbrandt, R. J. Homer, and J. A. Elias. Early growth response gene 1-mediated apoptosis is essential for transforming growth factor beta1-induced pulmonary fibrosis. J Exp Med 2004;200:377-389.
  • Noble, P. W., and R. J. Homer. Idiopathic pulmonary fibrosis: new insights into pathogenesis. Clin Chest Med 2004;25:749-58, vii.
  • Zhu, Z., T. Zheng, R. J. Homer, Y. K. Kim, N. Y. Chen, L. Cohn, Q. Hamid, and J. A. Elias. Acidic mammalian chitinase in asthmatic Th2 inflammation and IL-13 pathway activation. Science 2004;304:1678-1682.

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