GLENDA TRUJILLO, PhD
Glenda Trujillo, PhD
Research Assistant Professor
Basic Science Tower, Level 9
Stony Brook Medicine
Stony Brook, NY 11794-8691
Tel: (631) 444-3940
Fax: (631) 444-3424
Immune and inflammatory events in the pathogenesis of idiopathic pulmonary fibrosis; in vivo murine models of lung injury; acute exacerbations of pulmonary fibrosis. Idiopathic pulmonary fibrosis (IPF) is a chronic lung disease marked by progressive deterioration of lung function that is ultimately fatal. IPF is characterized by severe alveolar destruction, inflammation of variable intensity, excessive deposition of extracellular matrix (ECM), and ultimate loss of normal lung architecture and function. Although the pathogenesis of IPF is not completely understood, a persistent fibroblast expansion and activation into myofibroblasts is considered the common final pathway in all fibrosing diseases. My research investigates the activation of other cell types that contribute to the myofibroblast population, which can be derived from bone marrow derived cells (fibrocytes) and lung epithelial structures via epithelial-mesenchymal transition (EMT). Specifically, it focuses on acute exacerbations of pulmonary fibrosis and the contributions of viral infections. To do this, we utilize the bleomycin murine model of pulmonary fibrosis as well as a human-SCID model established by the transfer of primary lung cells from IPF patients.
|Institution and Location||Degree||Year(s)||Field of Study|
|Lehigh University, Bethlehem, PA||B.S.||1998||Biochemistry, Social Psychology Minor|
|State University of New York at Stony Brook, NY
||Ph.D.||2004||Immunology and Pathology Tract of the
Molecular and Cellular Biology
|2010-present||Research Scientist: Lab of Richard Kew, Ph.D., Pathology Department, SUNY Stony Brook, NY|
|2006-09||Post-Doctoral Research: Lab of Cory Hogaboam, Ph.D., Pathology Department, University of Michigan, Ann Arbor, MI|
|2008||Visiting Research Scientist: Lab of Gabor Jarai, Ph.D and John Westwick, Ph.D., Division of Respiratory Diseases, Idiopathic Pulmonary Fibrosis (IPF) Group Novartis Institutes for BioMedical Research, Horsham, West Sussex, UK|
|2004-05||Post-Doctoral Research: Lab of Richard Kew, Ph.D., Pathology Department, SUNY Stony Brook, NY|
|1999-04||Doctoral Research: Lab of Richard Kew, Ph.D., Pathology Department, SUNY Stony Brook, NY|
|2007-08||Consultant: Lab of Richard R. Kew, Ph.D., Pathology Department, SUNY Stony Brook, NY|
|2006-09||Research Mentor: Program in Biomedical Sciences, University of Michigan, Ann Arbor, MI|
|2005||Instructor: Pathology for First-year Medical Students, SUNY Stony Brook, NY|
|2004-05||Post-Doctoral Teaching Assistant: Pathology for the Health-Related Professions (HBP310), SUNY Stony Brook, NY|
|2006||NIH Institutional Training Grant (T32) for Pulmonary Research (3 years)|
|2004||W. Burghardt Turner Postdoctoral Fellowship (2 years)|
|2004||National Science Foundation Postdoctoral Fellowship (1 year)|
|2000||SUNY Stony Brook Graduate Student Training Grant (2 years)|
|1999||W. Burghardt Turner Graduate Fellowship (5 years)|
|1997||Howard Hughes Undergraduate Research Grant (1 year)|
|1994||Lehigh University Academic Scholarship (4 years)|
|1999-present||Society for Leukocyte Biology|
|2003-05||SREB Doctoral Scholars Program (Southern Regional Educational Board)|
|Co-inventor on a Pending U.S. Patent (Serial Number of 61/258,293) with Novartis and The University of Michigan surrounding the work, “TLR9 as a Biomarker for Rapidly Progressive Forms of Idiopathic Pulmonary Fibrosis”.|
Peer Reviewed Publications:
DiMartino, S.J., A.B. Shah, G. Trujillo, and R.R. Kew. 2001. Elastase controls the binding of the vitamin D-binding protein (Gc-globulin) to neutrophils. A potential role in the regulation of C5a cochemotactic activity. Journal of Immunology 166: 2688-2694.
Trujillo, G. and R.R. Kew. 2004. Platelet-derived thrombospondin-1 is necessary for the vitamin D-binding protein (Gc-globulin) to function as a chemotactic cofactor for C5a. Journal of Immunology 173: 4130-4136.
Shah A.B., DiMartino, S.J., G. Trujillo, and R.R. Kew. 2006. Selective inhibition of the C5a chemotactic cofactor function of the vitamin D binding protein by 1,25(OH)2 Vitamin D3. Molecular Immunology 43: 1109-1115.
DiMartino, S.J., G. Trujillo, L.A. McVoy, Jianhua Zhang, and R.R. Kew. 2007. Upregulation of the Vitamin D Binding Protein (Gc-globulin) Binding Sites During Neutrophil Activation from a Latent Reservoir in Azurophil Granules. Molecular Immunology 44:2370-7.
Trujillo, G. and C.M. Hogaboam. Chemokines and Their Receptors in Fibrosis. 2007. The Receptors. Humana Press, pp. 295-317
Trujillo, G., E.C. O’Connor, S.L. Kunkel and C.M. Hogaboam. 2008. A Novel Mechanism for CCR4 in the Regulation of Macrophage Activation in Bleomycin-induced Pulmonary Fibrosis. American Journal of Pathology 172:1209-21.
Bhan U., G. Trujillo, K. Lyn-Kew, M. W. Newstead, X. Zeng, C.M. Hogaboam, A.M. Krieg, and T.J. Standiford. 2008. TLR9 Regulates Lung Macrophage Phenotype and Host Immunity in Murine Legionella Pneumonia. Infection and Immunity. 76:2895-904.
Joshi, A.D., D.J. Fong, S.R. Oak, G. Trujillo, K.R. Flaherty, F.J. Martinez, C.M. Hogaboam. 2009. IL-17 Mediated Immunopathogenesis in Experimental Hypersensitivity Pneumonitis. Am. J. Respir. Crit. Care Med. 179:705-16.
Lindell, D.M, G. Trujillo, J.J. Smit, S.B. Morris, L. Boon, K.A. Cavassani, C.M. Hogaboam, and N.W. Lukacs. 2010. CC Chemokine Receptor 4-Dependent Trafficking of Regulatory T Cells Limits Airway Hyperresponsiveness During Chronic Allergic Lung Disease. Submitted for publication.
Trujillo, G., A. Meneghin, K.R. Flaherty, L.M. Sholl, J.L. Myers, E.A. Kazerooni, B.H. Gross, S.R. Oak, A.L. Coelho, H. Evanoff, E. Day, G.B. Toews, A.D. Joshi, M.A. Schaller, B. Waters, G. Jarai, J. Westwick, S.L. Kunkel, F.J. Martinez and C.M. Hogaboam. 2010. TLR9 Differentiates Rapidly from Slowly Progressing Forms of Idiopathic Pulmonary Fibrosis. Science Translational Medicine Nov 10; 2(57).
Trujillo, G., A.J. Hartigan, and C. M. Hogaboam. 2010. T Regulatory Cells and Attenuated Bleomycin- induced Fibrosis in Lungs of CCR7- /- Mice. Fibrogenesis & Tissue Repair3:18.
Trujillo, G., D.M. Habiel, L. Ge, M. Ramadass, J. Zhang and R.R. Kew. 2010. Leukocyte chemotaxis to C5a/C5a des Arg in physiological fluids. Requirement for the vitamin D binding protein, thrombospondin-1 and its receptor CD36 for full chemotactic activity. In preparation.
Trujillo, G., and Cory M. Hogaboam. 2010. Elevated TLR9 expression in CCR4-deficient mice increases their susceptibility to bleomycin-induced pulmonary fibrosis in an acute exacerbation model of idiopathic pulmonary fibrosis. In preparation.