Glenda Trujillo, PhD

Glenda Trujillo, PhD
Research Assistant Professor
Basic Science Tower L9
Stony Brook University School of Medicine
Stony Brook, NY 11794-8691

Tel: (631) 444-3940
Fax: (631) 444-3424
Email: gtrujillo@notes.cc.sunysb.edu

Research Summary:
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, my research 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.

Education:
1998	B.S., Biochemistry, Social Psychology Minor,College of Arts and Sciences, Magna Cum Laude, Lehigh University, Bethlehem, PA
2004	Ph.D., Immunology and Pathology Tract of the Molecular and Cellular Biology, State University of New York at Stony Brook, NY

Research Experience:

2010 - present	Research Scientist: Laboratory of Richard R. Kew, Ph.D. Department of Pathology, State University of New York at Stony Brook, NY Research Project 1: In vivo effect of the Vitamin D Binding Protein (DBP) on neutrophil chemotaxis in murine models of complement-dependent inflammation
2006 - 2009	Post-Doctoral Research: Laboratory of Cory M. Hogaboam, Ph.D. Department of Pathology, University of Michigan at Ann Arbor, MI Research Project 1: Role of CCR4 and its ligands in mediating the inflammatory component of the development of bleomycin-induced pulmonary fibrosis in mice. Research Project 2: Regulatory T cell trafficking and function in bleomycin-induced pulmonary fibrosis in mice. Research Project 3: Role of Toll-like receptor activation during bleomycin-induced injury in mice. Research Project 4: Cellular mechanisms that mediate acute exacerbations using unmethylated CpG in a humanized SCID mouse model of IPF. Research Project 5: In vitro studies with primary human lung fibroblasts cultured from IPF lung biopsies for protein and gene array analysis (in collaboration with Novartis Pharmaceuticals).
2008	Visiting Research Scientist: Laboratory 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 Research Project 1: Design of an in vitro model for the investigation of epithelial-to-mensenchymal transdifferentiation (EMT) by primary human blood monocytes. Research Project 2: Directed the completion of a collaboration with U of M for the identification of a novel cell-specific therapeutic IPF target using primary human fibroblasts cultured from IPF human lung biopsies.
2004 - 2005	Post-Doctoral Research: Laboratory of Richard R. Kew, Ph.D. Department of Pathology, State University of New York at Stony Brook, NY Research Project: Mechanism by which CD36 and/or CD47 function as thrombospondin-1 (TSP-1) receptors in the vitamin D-binding protein (DBP) co-chemotactic signaling complex for C5a-directed chemotaxis.
1999 - 2004	Doctoral Research: Laboratory of Richard R. Kew, Ph.D. Department of Pathology, State University of New York at Stony Brook, NY Dissertation Title: The C5a Chemotactic Cofactor Function of the Vitamin D Binding Protein (Gc) is Regulated by Thrombospondin-1 and CD36.

Teaching Experience:

2007 - 2008	Consultant: Laboratory of Richard R. Kew, Ph.D. Department of Pathology, State University of New York at Stony Brook, NY Consultant on mouse models of inflammation to investigate mechanisms of a novel chemotactic cofactor for C5a Trained the PI and members of the laboratory on mouse survival surgery techniques, tissue dissection and cell isolation and culture
2006 - 2009	Research Mentor: Program in Biomedical Sciences, University of Michigan, Ann Arbor, MI Supervised a first-year doctoral student in a hypothesis-driven research project for 3 months Delegated small research projects to undergraduate research students
2005	Instructor: Pathology for First-year Medical Students, State University of New York at Stony Brook, NY Organized and led discussions for interactive sessions in Immunology in a class of 25-30 medical students Prepared immunological scenarios for problem solving
2004 - 2005	Post-Doctoral Teaching Assistant: Pathology for the Health-Related Professions (HBP310), State University of New York at Stony Brook, NY Conducted pre-exam review sessions for Nursing and Physician Assistant students Individually tutored students

Awards:
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)

Professional Memberships:
1999-present	Society for Leukocyte Biology
2003-2005	SREB Doctoral Scholars Program (Southern Regional Educational Board)

Patents:
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”.

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).
Abstract
Reprint
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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.

Presentations at National/International Scientific Meetings:

Trujillo, G., A.J. Hartigan, and C.M. Hogaboam. T Regulatory Cells are Central to the Protective Effect Against Bleomycin-Induced Pulmonary Fibrosis Observed in CCR7-deficient Mice. International Colloquium on Lung Fibrosis, Myrtle Beach, North Carolina, September 28-October 1, 2008; Keystone Symposia Joint Meeting: Fibrosis and Allergy and Asthma, Keystone Resort, Colorado, January 20-25, 2009.

Trujillo, G., A.J. Hartigan, E.C. O’Conner and C.M. Hogaboam. CCR4-deficient Mice are Susceptible to CpG Challenge in an Acute Exacerbation Model of Bleomycin-induced Fibrosis as a Result of Phenotypic Changes in Macrophage Polarization. Experimental Biology, San Diego, California. April 5-10, 2008.

Trujillo, G., and C.M. Hogaboam. Phenotypic Differences in Alveolar Macrophages Confer the Attenuation of Bleomycin-Induced Pulmonary Fibrosis in CCR4-/- Mice. Keystone Symposia, The Macrophage: Homeostasis, Immunoregulation and Disease, Copper Mountain Resort, Colorado, April 11-16, 2007.

Trujillo, G., and C.M. Hogaboam. CCR4-Deficient Mice in a Bleomycin-induced Model of Pulmonary Fibrosis: Investigating the Role of CCR4 in the Balance Between Inflammation and Tissue Remodeling. International Colloquium on Lung Fibrosis, Eltville-Erbach, Germany, September 7-11, 2006.
Society for Leukocyte Biology, San Antonio, Texas, November 8-12, 2006.

Trujillo, G., and R.R. Kew. C5a Chemotactic Cofactor Function of the Vitamin D Binding Protein (DBP) Is Dependent on the Formation of a Novel Multifaceted Cell Surface DBP Binding/Signaling Complex. 10th European Meeting on Complement and Disease, Heidelberg, Germany, September 9-13, 2005.

Trujillo, G., and R.R. Kew. C5a Chemotactic Cofactor Function of the Vitamin D Binding Protein: Insight into the cellular mechanism using U937 cells transfected with the C5a receptor. 36th Annual Meeting of the Society for Leukocyte Biology, Philadelphia, PA, October 2-5, 2003.

Trujillo, G., and R.R. Kew. Identification of a Modified Form of the Vitamin D Binding Protein (DBP) That Functions as a Co-Chemotactic Factor for C5a. A Joint Meeting of the International Cytokine Society and Society for Leukocyte Biology, Maui, HI, November 8-11, 2001.