Anthony A. Azenabor, Ph.D., C.S., ASCP 

Associate Professor 

Interests and Expertise
My current research is aimed at providing greater insights into signal transductional mechanisms accounting for macrophage function following stimulation by physiological or 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 bacteria, pathogenic protozoa, fungi, worms and tumors especially those with potentials for metastasis. There are therefore two models around which my research efforts revolve. One model explores the interactions between Chlamydia pneumoniae and macrophages and the atherogenic consequences of interactions, while the other model investigates the effect of the female hormone, estrogen (17?-estradiol) on macrophage functions. Chlamydia pneumoniae becomes chronic in macrophage and renders macrophage atherogenic.

The model examining the interaction of macrophage with C. pneumoniae, a chronic respiratory intracellular pathogen provides the opportunity for us to explore the survival mechanism of C. pneumoniae in macrophage despite the endowment of the later with elaborate immune arsenals. The efforts in our laboratory are geared towards providing mechanistic explanations for the survival and chronic course of C. pneumoniae in host and demonstrating the biochemical links of C. pneumoniae infection with atherogenic process. We find the infection of macrophage by C. pneumoniae of central importance in the process. Emerging data from our laboratory are providing insights into how C. pneumoniae becomes chronic in macrophage via the regulation of Ca2+ influx signals in macrophage. The important implication of these aspects of our studies is that we think we now understand to prevent C. pneumoniae chronicity (probably, intracellular bacterial chronicity) and C. pneumoniae induced atherogenesis. Estrogen modifies macrophage functions.

The estradiol model of our research provides a unique opportunity for demonstrating how a physiological activator of macrophage modulates the signaling mechanism in operation when macrophage produces substances that have been known to affect their immune effector and regulatory functions. Evidences abound that estradiol mediated elaboration of reactive oxygen species in macrophage have beneficial signaling effect rather killing effect. The relevance of these findings is that our knowledge of the normal function of activated macrophage in non-disease state is profoundly enriched, we can therefore speculate about changes required to bring about more effective function in disease state.

Awards
International Society for Infectious Disease Award, 1997

Natural Sciences and Engineering Research Council of Canada, Visiting Scientist Award, 1998

Shaw Scientist Award, 2003

College of Health Sciences Dean Research Award, 2004

Graduate School/UWM Foundation Research Award, 2004

Recent Publications
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., Kennedy, P., Akoachere, J.F. (2007). Reactive Oxygen Species Homeostasis Regulates 17ß-Estradiol Mediation of Low Density Lipoprotein Receptor Expression in Macrophages. Journal of Cell and Molecular Biology. (Accepted, in press).

Azenabor, A.A, Muili, K, Akoachere, J.F, Chaudhry, A. (2006). Macrophage antioxidant enzymes regulateChlamydia 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, Yang S, Job G, Adedokun O.O. (2005). Elicitation of reactive oxygen species in Chlamydia pneumoniae-stimulated macrophages: a Ca2+-dependent process involving simultaneous activation of NADPH oxidase and cytochrome oxidase genes. Medical Microbiology and Immunology. 194: 91-103

Azenabor, A.A., Yang, S., Job, G and Adedokun, O.O. (2004). Expression of iNOS gene in macrophages-stimulated with 17?-estradiol is regulated by free intracellular Ca2+. Biochemistry and Cell Biology. 82(3): 381-390.

Azenabor, A.A., Job, G and Yang, S. (2004). Induction of lipoprotein lipase gene expression in Chlamydia pneumoniae-infected macrophages is dependent on Ca2+ signaling events. Biological Chemistry. 385: 67-74

Azenabor, A.A., Chaudhry, A.U and Yang, S. (2003). Macrophage L-type Ca2+ channel antagonists alter Chlamydia pneumoniae MOMP and HSP-60 mRNA gene expression, and improve antibiotic susceptibility. Immunobiology. 207(4): 237-245.

Azenabor, A.A. and Chaudhry, A.U. (2003). Chlamydia pneumoniae survival in macrophages is regulated by free Ca2+ dependent reactive nitrogen and oxygen species. Journal of Infect. 46(2): 120-128.

Azenabor, A.A. and Chaudhry, A.U. (2003). Effective macrophage redox defense against Chlamydia pneumoniae depends on L-type Ca2+ channel activation. Medical Microbiology and Immunology. 193: 99-106.

Speaker Topics 
Chlamydia pneumoniae
Immunology
Medical Parasitology and Mycology
Diagnostic Virology
Microbial Pathogenesis

Education
Ph.D., University of Benin, Pathogenic Microbiology, 1992
M.S., University of Benin, Biochemistry, 1988