Anthony A. Azenabor, Ph.D., C.S (ASCP)
- Chlamydial Pathogenesis
- Host-Pathogen Interactions
Enderis Hall, Room 459
Phone: (414) 229-5637
Fax: (414) 229-2619
- 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
Interests & Expertise
My expertise is in Infectious Diseases and Immunity. In my research, I have approached this subject by explaining the impact of infection on host immune system, relying on my knowledge of Molecular Biochemistry as a major tool. My current 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 host defense against pathogens and other challenges.
There are two models around which my 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 for us 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.Back to the top
- 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
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.
Azenabor, A.A., Muili, K, Akoachere, J.F, Chaudhry, A. (2006). Macrophage Antioxidant Enzymes Regulate Chlamydia pneumoniae Chronicity: evidence of the effect of redox balance on host-pathogen relationship. Immunobiology, 211, 325-339.
Azenabor, A.A., Job, G, Adedokun, O.O. (2005). Chlamydia pneumoniae -Infected Macrophages Exhibit Enhanced Plasma Membrane Fluidity and Show Increased Adherence to Endothelial Cells. Molecular and Cellular Biochemistry, 269, 69-84.
Azenabor, A.A., Job, G and Yang, S. (2004). Induction of Lipoprotein Lipase Gene Expression in Chlamydia pneumoniae -Infected Macrophages is Dependent on Ca 2+ Signaling Events. Biological Chemistry, 385, 67-74.
Azenabor, A.A., Chaudhry, A.U and Yang, S. (2003). Macrophage L-type Ca 2+ Channel Antagonists Alter Chlamydia pneumoniae MOMP and HSP-60 mRNA Gene Expression, and Improve Antibiotic Susceptibility. Immunobiology, 207(4), 237-245.