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Edward Sherwood, MD, PhDEdward Sherwood, MD, PhD
Professor
Departments of Anesthesiology and Microbiology & Immunology


Phone: (409)772-1221
Email: ersherwo@utmb.edu

Education: MD, 1994, University of Chicago
PhD, 1986, Tulane University
BS, 1981, Southwestern University

Overview: Immunopathogenesis of sepsis, innate immunity

Research Interests

We demonstrated that ß2 microglobulin knockout mice that are depleted of natural killer (NK) cells by treatment with anti-asialoGM1 exhibit decreased systemic inflammation, less metabolic acidosis, reduced hypothermia, better hemodynamic function and improved survival compared to control mice following cecal ligation and puncture (CLP). ß2MKO/aAsGM1 mice have multiple immunological defects including an absence of CD8+ T, natural killer (NK) and natural killer T (NKT) cells as well as deficient expression of the class I major histocompatability complex (MHC-I) and CD1 molecules. Our recent ?ndings strongly support the contention that depletion of CD8+ T and NK cells are the primary factors providing protection from CLP-induced injury in ß2MKO/aAsGM1 mice.

Most recently, we have focused on the contributions of NK cells to the pathogenesis of septic shock caused by cecal ligation and puncture. Our recent studies show that large numbers of NK cells migrate from spleen and blood into the peritoneal cavity where they facilitate the activation of myeloid cells. We are studying the mechansisms that regulate NK cell trafficking during sepsis and the mechanisms utilized by NK cells to facilitate myeloid cell activation.

Another major interest in my laboratory is altered antimicrobial immunity in experimental models of sepsis and thermal injury. Our goal is to identify the cellular and molecular changes that result in altered antimicrobial immunity in these models and to develop treatment approaches to decrease infectious complications in these patient populations. We are currently investigating several immunomodulatory strategies including the use of microbial immunomodulators such as glucan and monophosphoryl lipid A to prime innate and acquired responses to opportunistic pathogens such Pseudomonas aeruginosa. We are also studying the hemeopoietic factor FLt-3 ligand, which preferentially induces dendritic cell generation and differentiation. Out studies show that Flt-3 ligand will stimulate antimicrobial immune responses in models of post-injury immunosuppression.

Recent Publications

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