Chlamydia trachomatis infection induces mucosal addressin cell adhesion molecule-1 and vascular cell adhesion molecule-1, providing an immunologic link between the fallopian tube and other mucosal tissues
Ka. Kelly et al., Chlamydia trachomatis infection induces mucosal addressin cell adhesion molecule-1 and vascular cell adhesion molecule-1, providing an immunologic link between the fallopian tube and other mucosal tissues, J INFEC DIS, 184(7), 2001, pp. 885-891
The development of a protective vaccine against the sexually transmitted di
sease caused by Chlamydia trachomatis may prevent complications associated
with insidious infection. Vaccination via the vaginal route may not be prac
tical, and other routes should be investigated. To this end, the adhesion m
olecules induced on the fallopian tube endothelium during infection with C
trachomatis were characterized. Adhesion molecules were identified in fallo
pian tube biopsy specimens cultured with 5 x 10(6) infection-forming units
of C trachomatis serovar E. Frozen sections were prepared from these tissue
s and were stained by immunohistochemical techniques. Infection with live,
but not UV-inactivated, C trachomatis induced a significant increase in lev
els of vascular cell adhesion molecule-1 and the mucosal addressin cell adh
esion molecule-1 but not of other adhesion molecules. Therefore, infection
with C trachomatis induces adhesion molecules that are associated with othe
r mucosal tissues and inflammatory sites, which suggests that mucosal route
s of immunization may be effective.