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Antimicrobial Agents and Chemotherapy, 06 1997, 1335-1344, Vol 41, No. 6
PB Wyrick, ST Knight, DG Gerbig Jr, JE Raulston, CH Davis, TR Paul and D Malamud
Safe and effective vaginal microbicidal compounds are being sought to offer
women an independent method for protection against transmission of sexually
acquired pathogens. The purpose of this study was to examine the efficacy
of two formulations of one such compound, C31G, against Chlamydia
trachomatis serovar E alone, its host epithelial cell (HEC-1B) alone, and
against chlamydiae-infected HEC-1B cells. Preexposure of isolated, purified
infectious chlamydial elementary bodies (EB) to C31G, at pHs 7.2 and 5.7,
for 1 h at 4 degrees C resulted in reduced infectivity of EB for HEC-1B
cells. Examination of the C31G-exposed 35S-EB on sodium dodecyl
sulfate-polyacrylamide gel electrophoresis autoradiographs and by Western
blotting revealed a C31G concentration-dependent and pH-dependent
destabilization of the chlamydial envelope, resulting in the release of
chlamydial lipopolysaccharide and proteins. Interestingly, when the host
human genital columnar epithelial cells were infected with chlamydiae and
then exposed to dilute concentrations of C31G which did not alter
epithelial cell viability, chlamydial infectivity was also markedly
reduced. C31G gained access to the developing chlamydial inclusion causing
damage to or destruction of metabolically active reticulate bodies as well
as apparent alteration of the inclusion membrane, which resulted in
premature escape of chlamydial antigen to the infected epithelial surface.
These studies show that the broad-spectrum antiviral and antibacterial
microbicide C31G also has antichlamydial activity.
Copyright © 1997 by the American Society for Microbiology. All rights reserved.
The microbicidal agent C31G inhibits Chlamydia trachomatis infectivity in vitro
Department of Microbiology and Immunology, University of North Carolina- Chapel Hill School of Medicine, North Carolina, 27599-7290, USA. pbwyrick@med.unc.edu
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