Anthony A. Azenabor, Ph.D., C.S (ASCP)
Enderis Hall, Room 459
- Department of Medical Microbiology and Immunology
University of Wisconsin Medical School Madison, WI, 2000 – 2001
- Immunology Laboratories Department of Health Studies
University of Waterloo, Waterloo, Ontario, Canada, 1998 – 2000
- Regional Virology and Chlamydiology Laboratories
McMaster University, Hamilton, Ontario, Canada, 1996 -1998
- Department of Biochemistry, University of Benin
Benin City, Nigeria, 1993 -1996
- Ph.D., University of Benin, 1992
- Chlamydial Pathogenesis
- Host-Pathogen Interactions
Dr. Azenabor’s expertise is in Infectious Diseases and Immunity. He approaches the subject by explaining the impact of infection on host immune system, relying on knowledge of Molecular Biochemistry as a major tool. His research is aimed at providing greater insights into mechanisms involved in macrophage function during stimulation by both physiologic and infectious agents. The macrophages are important cells of the immune system, involved in all stages of immune response. Products of their activation account wholly or in part for ho
There are two models around which Dr. Azenabor’s research efforts revolve. One model explores the interactions between Chlamydia pneumoniae or Chlamydia trachomatis and macrophages and the consequences of such interactions on body functions, while the other model investigates the effect of the female hormone, 17-beta estradiol, on macrophage functions.
The model examining the interaction of macrophage with C. pneumoniae or C. trachomatis, both chronic intracellular pathogens, provides the opportunity for us to explore the survival mechanism of chlamydia in macrophage. The efforts in our laboratory have provided insights into the biochemical links of C. pneumoniae infection with atherogenic process, and possible involvement of C. trachomatis in miscarriages and abortions.
The estradiol model of our research shows that estrogen modifies macrophage functions. This model has provided a unique opportunity to demonstrate how a physiological activator (estrogen) can modulate macrophage functions. Evidences abound that estradiol mediated elaboration of reactive oxygen species in macrophage have beneficial signaling effect rather killing effect. These findings enrich our knowledge of the normal function of activated macrophage in non-disease state.
Azenabor, A. A., Cintron-Cuevas, J., Schmitt, H., & Bumah, V. (2011). Chlamydia trachomatis Induces Anti-inflammatory Effect in Human Macrophages by Attenuation of Immune Mediators in Jukat T-cells. Immunobiology, 216, 1248-1255.
Azenabor, A. A., & York, J. (2010). Chlamydia trachomatis Evokes a Relative Anti-inflammatory Response in a Free Ca 2+ - Dependent Manner in Human Macrophages. Comparative Immunology Microbiology and Infectious Diseases, 33, 513-528.
Azenabor, A. A., Kennedy, P., & York, J. (2009). Free Intracellular Ca 2+ Regulates Bacterial Lipopolysaccharide Induction of iNOS in Human Macrophages. Immunobiology, 214, 143-152.
Azenabor A. A., Kennedy, P., & Balistreri, S. (2007). Chlamydia trachomatis Infection of Human Trophoblast Alters Estrogen and Progesterone Biosynthesis: an insight into role of infection in pregnancy sequelae. International Journal of Medical Sciences, 4(4), 223-231.
- International Society for Infectious Disease Award
- Natural Sciences and Engineering Research Council of Canada, Visiting Scientist Award
- Shaw Scientist Award
- College of Health Sciences Dean Research Award
- Graduate School/UWM Foundation Research Award