CHS Office of Research

Ismail El-Amouri

Ismail EL-Amouri completed his B.S. (Hons) in Medical Technology, in the College of Health Sciences at UK in 2000. Later in the same year, he became a certified member of the American Society for Clinical Pathology (ASCP).

He worked at Saint Joseph Hospital for few years, where he gained excellent experience and knowledge in chemistry, blood banking, hematology and microbiology, as well as in disease analysis and diagnosis. During his professional carrier, he became fascinated with the science of hematology for its central role in keeping us alive.

To purse his dream of becoming a doctor in hematology, he attended the doctoral program of hematology/transplantation in the department of Clinical Sciences at UK in 2004. Currently, Mr. EL-Amouri is a research assistant (RA) in Dr. Oakley’s lab working on his doctorate project, hoping to contribute to the medical field in particular and to society in general. In December of 2006, he presented his on-going research at the 35th Autumn Immunology conference (AIC) in Illinois, Chicago.

Ismail's Research Abstract

The role of decay accelerating factor (DAF) and Murine Cytomegalovirus (MCMV) in bone marrow transplantation (BMT)

Ismail S. EL-Amouri, Mohammad A. Bani-Ahmad, Oliver R. Oakley

Division of hematology/transplantation, Department of Clinical Sciences, College of Health Sciences, University of Kentucky, Lexington, KY

Allograft rejection induced by cytomegalovirus (CMV) remains the main obstacle toward a successful long-term transplant survival. Many clinical studies have shown a direct correlation between cytomegalovirus (CMV) infection and allograft rejection. Host innate immunity is the first line of defense against invaders.

The complement system is a vital part of host innate immunity that consists of many serum and membrane-bound proteins that interact in a sequential manner to defend the host from pathogens such as CMV. The complement system is also regulated at different levels by both soluble and membrane-bound regulatory proteins to maintain a homeostasis environment.

Decay accelerating factor (DAF), also known as CD55, is a membrane-bound regulatory protein that controls C3 complement protein, the central component of the complement system that provides an imperative link between the innate and adaptive immune systems. DAF is widely expressed on cells both within and outside the vascular system. The main function of DAF is to protect autologous cells from complement-mediated cytolysis but it also plays a role in T-cell activation.

The protective role of DAF in xenotransplantation has been extensively researched to prevent rejection of transgenic organ transplant. The pathogenesis of graft rejection consists of complex immunological and non-immunological mechanisms. Humoral as well as cell-mediated immune reactions have been implicated in allograft rejection. Although primarily driven by T-cell responses the role of complement activation in acute allograft rejection has become evident in recent years. Activation of the humoral branch of the immunological responses plays a crucial role in the pathogenesis of chronic rejection suggesting a pivotal role of complement activation in chronic allograft rejection.

Our preliminary data have shown that mice previously infected with sublethal dose of MCMV followed by bone marrow transplant have reduced expression of CD55 when compared to uninfected mice, indicating that MCMV may accelerate graft versus host disease (GVHD) by interfering with surface CD55 expression ultimately exposing the graft to complement attack. Understanding the contribution of MCMV to graft rejection and the role of DAF will aid in the development of new strategies for preventing GVHD in BMT patients.

Ismail El-Amouri
PhD Candidate, UK College of Health Sciences, Clinical and Reproductive Sciences. Focus: Hematology / Transplantation