of Oklahoma, Ph.D. 1988
Fidel received his Bachelor of Science degree in
Biology from Allegheny College in Pennsylvania
in 1984. He then received his Master of Science
and PhD degrees in Microbiology from the
University of Oklahoma in 1987 and 1988,
respectively. Dr. Fidel conducted postdoctoral
training in the lab of Dov Boros in the
Department of Immunology and Microbiology at
Wayne State University School of Medicine in
Detroit. He accepted a position of Assistant
Professor in the Division of Infectious
Diseases, Department of Internal Medicine, Wayne
State University School of Medicine in 1990. Dr.
Fidel came to LSUHSC in 1995 as an associate
professor in the Department of Microbiology,
Immunology, and Parasitology. He was promoted to
professor in 1999 and named the Carl Baldridge
Research Professor and Director of the Center of
Excellence in Oral and Craniofacial Biology,
Associate Dean for Research in 2001. He was
named interim chair of the new Department of
Oral and Craniofacial Biology in 2007 and
permanent chair of the department in
2009. In 2013 Dr. Fidel became course director of the advanced education research methodologies course.
the Associate Dean of Research and Director of
the Center of Excellence, Dr. Fidel also
oversees all research conducted at the dental
school. He has served as Principal Investigator of a
$10.7 million Center of Biomedical Research
Excellence (COBRE) grant from the NIH (National
Center for Research Resources-NCRR) for the
dental school to develop promising junior
faculty into independent researchers. He has also
served as Principal Investigator of the $3.35
million grant from the LA Board of Regents to
establish a South Louisiana Institute of
Infectious Disease Research.
Fidel laboratories have been funded under
several sources from the NIH, including the
National Institute for Dental and Craniofacial
Research (NIDCR) and the National Institute for
Allergy and Infectious Diseases (NIAID). Studies
in the Fidel laboratory focus on host defense
against mucosal infections caused by the fungus,
Candida albicans. Research in vaginal
candidiasis is in both humans and
animal models. The research has recently
revealed a paradigm shift away from adaptive
immune deficiencies as a cause of infection to
innate immune mechanisms playing a role in both
susceptibility and resistance to infection.
Research in oral candidiasis is
focused in HIV-infected individuals. This
research is focused on the protective role of
CD8 T cells and the role of microbiome in the pathogenesis of disease. In addition oral and vaginal
epithelial cell antifungal immune mechanisms are
being studied. Finally, the role of vaginal and
oral Candida biofilms in the pathogenesis of
vaginitis and denture stomatitis is being
studied through a collaboration with the Noverr
Iimmunopathogenesis of recurrent vaginal or
Mucosal microbiome in disease pathogenesis
Lilly, E.A, J. Yano, and P.L. Fidel, Jr. (2010). Annexin–A1 Identified as the oral epithelial cell anti-Candida effector moiety. Mol Oral Micro. 25:293-304.
Yano, J., E.A. Lilly, M.E. Barousse, and P.L. Fidel, Jr. (2010). Epithelial cell-derived S100 calcium-binding proteins as key mediators in the hallmark acute neutrophil response during Candida vaginitis. (Infect. Immun. 78:5126-513.
Lee, H, A. Yu, C. Johnson, M.C. Noverr, and P.L. Fidel, Jr. (2011). Fabrication of a removable intraoral denture device for rodent models of biofilm research. J. Oral Rehab. 38:686-690.
Quimby, K, E. A. Lilly, M. Zacharek, K. McNulty, J.E. Leigh, J.E. Vazquez, and P.L. Fidel, Jr. (2012) CD8 T cells and E-cadherin in host responses against oropharyngeal candidiasis. Oral Dis. 18:153-161.
Yano, J., J.K. Kolls, K.I Happel, F.W. Wormley, Jr., K.L. Wozniak, and P.L. Fidel, Jr., (2012). The acute neutrophil response mediated by S100 alarmins during vaginal candidiasis is independent of the Th17 pathway. Plos One 7(9) e46311.
Yano, J., M.C. Noverr, and P.L. Fidel, Jr. (2012) Cytokines in the host response to Candida vaginitis: Identifying a role for non-classical immune mediators, S100 alarmins. Special issue: Cytokines in fungal immunity. Cytokine 58:118-128.
Yano, J, Palmer, G., K. Eberle, T. Vogl, A. McKenzie, and P.L. Fidel, Jr. (2014) Vaginal epithelial cell-derived S100 alarmins induced by C. albicans via pattern recognition receptor interactions is sufficient but not necessary for the acute neutrophil response during experimental vaginal candidiasis. Infect. Immun. 82(2):783-792.
Peters, B.M., G. Palmer, P.L. Fidel, Jr. and M.C Noverr. (2014) Fungal morphogenetic pathways are required for the hallmark inflammatory response during Candida vaginitis. Infect. Immun. 82(2):532-543
Nash, E., B Peters, G. Palmer, P.L. Fidel, Jr., and M.C. Noverr. (2014). Morphogenesis is not required for Candida albicans-Staphylococcus aureus intra-abdominal infection-mediated dissemination and lethal sepsis. Infect. Immun., 82(8):3426-35.
Bruno, V.M., A.C. Shetty, J. Yano, P.L. Fidel, Jr., M.C. Noverr, B.M Peters. (2015) Transcriptomic analysis of vulvovaginal candidiasis identifies a role for the NLRP3 inflammasome. MBio 6(2):e00182-15
Garvey, E.P., W.J. Hoekstra, R.J. Schotzinger, J.D. Sobel, E.A. Lilly, and P.L. Fidel, Jr. (2015) Efficacy of the clinical agent VT-1161 against fluconazole-sensitive and –resistant Candida albicans in a murine model of vaginal candidiasis. Antimicrob. Agents Chemother 59(9):5567-73