6 / 6
S e p t e m b e r 1 0 - 1 1 , 2 0 1 8 | D u b l i n , I r e l a n d
Cell and Gene Therapy 2018 & Clinical Microbiology Congress 2018
Page 18
allied
academies
CLINICAL AND MEDICAL MICROBIOLOGY
CELL AND GENE THERAPY
&
World Congress on
International Conference on
Joint Event on
Biomedical Research
|
ISSN: 0976-1683
|
Volume 29
James Mahony, Biomed Res 2018, Volume 29 | DOI: 10.4066/biomedicalresearch-C3-006
INTRANASAL VACCINATION WITH THE
TYPE III SECRETION SYSTEM (T3SS)
ANTIGEN BD584 REDUCES BOTH
VAGINAL SHEDDING OF
CHLAMYDIA
TRACHOMATIS
AND ASSOCIATED UPPER
GENITAL TRACT PATHOLOGY
C
hlamydia trachomatis
infections are themost prevalent sexually transmitted
bacterial infections in the world. The WHO has estimated that there are 131
millionnewcasesevery year and recently it hasbeenshown that prior Chlamydia
infection is associated with increased risk of ovarian cancer. With up to 90% of
women and 50% of men having asymptomatic infections many infections go
undiagnosed and untreated leading to complications in women including pelvic
inflammatory disease (PID), tubal factor infertility and ectopic pregnancy. Public
health programs, including screening, partner identification and treatment have
failed to curb infection rates indicating the need for an effective vaccine. We
have shown previously using a mouse challenge model that vaccination with
the BD584 antigen protected mice against
C muridarum
and reduced both
bacterial shedding in the vagina and upper genital tract (UGT) pathology. We
have now extended these findings to investigate whether BD584 protects
against
C trachomatis
infection. C57BL/6 mice were vaccinated intranasally
with BD584 and CpG adjuvant (BD584/CpG) then challenged intravaginally with
C trachomatis
. BD584 vaccination elicited serum neutralizing antibody, vaginal
antibody and cell-mediated immune responses consistent with a Th1 polarized
immune response (INFγ, IL-17 and IgG2a/c:IgG1 antibody ratio). Vaccinated
mice had reduced vaginal shedding and reduced UGT pathology (uterine horn
dilation and hydrosalpinx) providing evidence that vaccination can protect
against late sequelae following resolution of a
C trachomatis
infection. We will
also present data on a novel delivery method for the BD584 vaccine involving
genetically engineered bacteria. We are currently investigating the efficacy of
the BD584 vaccine in a second animal model and if the vaccine is effective in
the piglet model then these results would strengthen the rationale for the use
of BD584 T3S proteins in a human vaccine and a phase I human trial.
Biography
James Mahony is currently working as a Professor
Emeritus in Pathology and Molecular Medicine at
University of Toronto, Canada. He is teaching with-
in the faculty of health sciences includes medical
microbiology/infectious diseases and pathology
residency training programs, graduate course in
clinical virology (MS763) and medical sciences.
He completed his fellowship in Microbiology at
American Academy of Microbiology as well as in
Canadian College of Microbiology. He has deco-
rated his carrier with several publication with lo-
cal, international, industrial collaboration with Drs
Mark Loeb, Jenny Johnstone, Marek Smieja, Peter
Timms (Brisbane), Phil Hansbro (Newcastle, Aus-
tralia), Lee Ann Campbell (Seattle), Theo Moraes
(Toronto) and Luminex Molecular Diagnostics, Qia-
gen, Pro-L. The major focus area of his research is
the pathophysiology of acute respiratory infections
caused by specific viruses (influenza, RSV) and
bacteria (Chlamydia pneumoniae, P aeruginosa
and C difficile). One of the major focuses of his
laboratory is the development of new antimicrobial
agents for both respiratory viruses and bacteria. In
addition to the development of novel therapeutics
the other focus of his clinical research is in the ar-
eas of diagnostics.
mahonyj@mcmaster.caJames Mahony
McMaster University, Canada