Jorge E. Albina Professor of Surgery

Dr. Jorge E. Albina is Professor of Surgery and Director of Surgical Research at Rhode Island Hospital/Alpert Medical School of Brown University, and Director of Nutritional Support Services, Department of Surgery, Rhode Island Hospital.

As Alpert Medical School faculty, Dr. Albina instructs the Surgical Nutrition Rotation, Surgical Residency Program, Nutrition Surgical Core Clerkship Course, Basic Science in Surgery, and the Integrated Program in Surgery.

A faculty member of the Graduate Program in Pathobiology, Dr. Albina is actively engaged in teaching undergraduates, graduates and Alpert Medical School students and has served as Doctoral Thesis Advisor and Doctoral Thesis Committee Member.

Dr. Albina is also a Faculty Sponsor for Brown University's Summer Research Early Identification Program, which is funded by the NIH Short Term Training for Minority Students grant and The Leadership Alliance. He is also the Principal Investigator on a T32 Trauma & Inflammation Research Training grant.

As Director of Surgical Research, Dr. Albina has authored over 70 peer-reviewed manuscripts. His research area of expertise is wound healing and inflammation, with emphasis on clinical applications that will allow active therapeutic intervention.

Dr. Albina is a frequently requested reviewer for many peer-reviewed journals. He is a renowned speaker, with over 200 invited presentations worldwide.

Brown Affiliations

Research Areas

scholarly work

Crane M.J., Daley J.M., van Houtte O., Henry W.L., Brancato S.K., and Albina J.E.  The monocyte to macrophage transition in the sterile wound. PLoS ONE, 9(1):e86660. doi:10.1371/journal.pone.0086660, 2014.

Brancato, S.K., Thomay, A.A., Albina, J.E., Reichner, J.S., Sabo, E., and Daley, J.M.  TLR4 signaling regulates the acute local inflammatory response to injury and the fibrosis/neovascularization of sterile wounds.  Wound Repair and Regeneration, 21(4):624-633, 2013

Brancato, S.K., Albina, J.E. Wound macrophages as key regulators of repair: Origin, phenotype and function. American Journal of Pathology 178(1):19-25, 2011

Daley, J.M., Thomay, A.A., Reichner, J.S., and Albina, J.E. The phenotype of murine wound macrophages. Journal of Leukocyte Biology, 87:59-67, 2010

Thomay, A.A., Daley, J.M., Sabo, E., Worth, P.J., Shelton, L.J., Reichner, J.S., Albina, J.E. Disruption of interleukin-1 (IL-1) signaling improves the quality of wound healing. American Journal of Pathology 174:2129-2136, 2009.

Xu, J., Reichner, J.S., Mastrofrancesco, B., Henry Jr., W., Albina, J.E. Prostaglandin E2 inhibits lipopolysaccharide-induced type I IFN (IFNβ) production in murine J774A.1 macrophages. Journal of Immunology 180:2125-2131, 2008

Daley, J.M., Thomay, A., Connolly, M., Reichner, J. and Albina, J.E. Use of Ly6Gspecific monoclonal antibody to deplete neutrophils in mice. Journal of Leukocyte Biology 83:64-70, 2008.

Lavigne, L.M., O'Brien, X.M., Kim, M., Janowski, J. W., Albina, J.E., Reichner, J.S. Integren engagement mediates the human PMN leukocyte response to a fungal pathogen-associated molecular pattern. Journal of Immunology 178:7276-7282, 2007

Lavigne, L., Albina, J.E., and Reichner, J.S. The effects of beta-glucan on adhesion-dependent human neutrophil functions. Journal of Immunology 177(12): 8667-75, 2006.

LeBlanc, B.W., Albina, J.E. and Reichner, J.S. The effect of PGG-β-glucan on neutrophil chemotaxis in vivo. Journal of Leukocyte Biology 79: 667-675, 2006.

Chung, A.S., Guan, Y-J., Yuan, Z-L., Albina, J.E., and Chin, Y.E. Ankyrin repeat and SOCS Box3 (ASB3) mediates ubiquitination and degradation of TNF Receptor-II. Molecular and Cellular Biology 25: 4716-4726, 2005.

Daley, J.M., Ivanenko-Johnston, T., Reichner, J.S., and Albina, J.E. Transcriptional regulation of TNF-α production in neutropenia. American Journal of Physiology: Regulatory, Integrative and Comparative Physiology 288:R409-R412, 2005

Din, Y., Chung, C.-S., Newton, S., Chen, Y., Carlton, S., Albina, J.E., and Ayala, A. Polymicrobial sepsis induces divergent effects on splenic and peritoneal dendritic cell function in mice. Shock, 22:137-144, 2005.

Daley, J.M., Reichner, J.S., Mahoney, E.J., Manfield, L., Henry, W.L., Jr., Mastrofrancesco, B., and Albina, J.E. Modulation of macrophage phenotype by soluble product(s) released from neutrophils. Journal of Immunology 174:2265, 2005.

Albina, J.E., Mahoney, E.J., Daley, J.M., Wesche, D.E., Morris, S.M., Jr. and Reichner, J.S. Macrophage arginase regulation by C/EBP/β. Shock 23:168-172, 2005.

Tsikitis, V.L., Albina, J.E., and Reichner, J.S. β-glucan affects leukocyte navigation in complex chemotactic gradients. Surgery, 136:384-389, 2004.

Tsikitis, V.L., Morin, N.A., Harrington, E.O., Albina, J.E., and Reichner, J.S. β-glucan protects endothelial barrier function from activated neutrophils. Journal of Immunology, 173:1284-1291, 2004.

Reichner, J.S. and Albina, J.E. Determination of the role of hypoxia-inducible factor 1 in wound healing. Methods in Enzymology,381:527-538, 2004.

research overview

Successful wound healing requires the coordinated activities of the multiple cell types that constitute the inflammatory and reparative response to tissue injury. The definition of the growth factors, cytokines, matrix components, and other products present in the wound that modulate wound healing-cell functions will allow a better understanding of the process of repair and promises clinical applications that will allow active therapeutic intervention. The development of these applications will require a better characterization of the phenotype and biology of inflammatory cells, most specifically as it relates to modulation by the wound environment.

research statement

The Surgical Metabolism laboratory is focused on the definition of the phenotypes of wound cells, and of the wound environment as a determinant of these phenotypes. Particular emphasis has been placed on the characterization of the wound macrophage phenotype and of the cellular and extracellular signals encountered by monocytes arriving at a site of injury that modulate their differentiation into wound healing macrophages.

funded research

1.   2004- 2014 Principal Investigator
Trauma and Inflammation Research Training
T32 GM065085-08
NIH/NIGMS Total Costs: $590,870

2.   2010- 2014 Collaborator
Programmed Cell Death: Role in Septic Immune Dysfunction
R01 GM053209-17
NIH/NIGMS Total Costs: $1,039,163

3.   2002– 2014 Collaborator
COBRE Center for Cancer Research Development
P20 RR017695-08
NIH/NCRR Total Costs: $5,796,728