Postdoc Training Medical Microbiology and Immunology University of Wisconsin-Madison 2001
Postdoc Training Immunology Laboratories University of Waterloo 2000
Postdoc Training Regional Virology and Chlamydiology Laboratories McMaster University 1998
Postdoc Training Biochemistry University of Benin 1996
Ph D Pathogenic Microbiology University of Benin 1993
MS Biochemistry University of Benin 1988
Fellow of the Institute of Medical Laboratory Sciences Hermatology and Blood Serology University of Benin 1985
Associate of the Institute of Laboratory Sciences Chemical Pathology University of Lagos 1981
- Chlamydial Pathogenesis
- Host-Pathogen Interactions
Interests & Expertise
Anthony 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 host defense against pathogens and other challenges.
There are two models around which 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 his 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 his 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.
George, Z., Omosun, Y., Azenabor, A. A., Partin, J., Joseph, K., Ellerson, D., He, Q., Eko, F., Bandea, C., Svoboda, P., Pohl, J., Black, C. M., & Igietseme, J. U. (2017). The Roles of Unfolded Protein Response Pathways in Chlamydia Pathogenesis. JOURNAL OF INFECTIOUS DISEASES
Azenabor, A. A. (2014). Immunology for the medical sciences: A practical approach.
Azenabor, A. A., Yang, S., Job, G., & Adedokun, O. O. (2005). Elicitation of reactive oxygen species in Chlamydia pneumoniae-stimulated macrophages: a CaP2+P-dependent process involving simultaneous activation of NADPH oxidase and cytochrome oxidase genes. Medical Microbiology Immunology, 194, 91-103.
Azenabor, A. A., Yang, S., Job, G., & Adedokun, O. O. (2004). Expression of iNOS gene in macrophages-stimulated with 17β-estradiol is regulated by free intracellular CaP2+P. Biochemistry and Cell Biology, 82(3), 381-390.
Azenabor, A. A., Job, G., & Yang, S. (2004). Induction of lipoprotein lipase gene expression in Chlamydia pneumoniae-infected macrophages is dependent on CaP2+P signaling events. Biological Chemistry, 385, 67-74.
Azenabor, A. A., Chaudhry, A. U., & Yang, S. (2003). Macrophage L-type CaP2+P channel antagonists alter Chlamydia pneumoniae MOMP and HSP-60 mRNA gene expression, and improve antibiotic susceptibility. Immunobiology, 207(4), 237-245.
Azenabor, A. A., & Chadhry, A. U. (2003). Effective macrophage redox defense against Chlamydia pneumoniae depends on L-type CaP2+P channel activation. Medical Microbiology and Immunology, 193, 99-106.
Azenabor, A. A., & Chaudhry, A. U. (2003). Chlamydia pneumoniae survival in macrophages is regulated by free CaP2+P dependent reactive nitrogen and oxygen species. Journal of Infect, 46(2), 120-128.
Honors & Awards
Fulbright Faculty Associate (2016) US Department of State.
Marquis Who’s Who in Medicine and Healthcare (2016) Who’s Who in Medicine and Healthcare.
DAAD Fellow (2008) German Academic Exchange Service Federal Ministry of Education, Republic of Germany.
Fulbright Faculty Associate (2005) US Department of State.
Nominee for Howard Hughes Medical Institute Investigators Competition Fulbright Faculty Associate (2005) University of Wisconsin–Milwaukee.
Dean’s Research Award (2004) College of Health Sciences, University of Wisconsin-Milwaukee.
Graduate School Research Award (2004) University of Wisconsin Foundation.
Greater Milwaukee Foundation Shaw Scientist Award (2003) University of Wisconsin-Milwaukee.
International Society for infectious Diseases (ISID) Scientist Award (1997) McMaster University Regional Virology Chlamydiology Laboratory St. Joseph’s Hospital Hamilton, Ontario, Canada.
University Research Project Committee (URPC) Award (1994) University of Benin.
Nigeria Scholarship for Doctoral Studies (1990) Department of Microbiology, University of Benin, Benin City.
Natural Sciences and Engineering (1988) University of Waterloo.