Chlamydia trachomatisInfection 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

Abstract

The development of a protective vaccine against the sexually transmitted disease caused by Chlamydia trachomatis may prevent complications associated with insidious infection. Vaccination via the vaginal route may not be practical, and other routes should be investigated. To this end, the adhesion molecules induced on the fallopian tube endothelium during infection with C. trachomatis were characterized. Adhesion molecules were identified in fallopian tube biopsy specimens cultured with 5 x 10(6) infection-forming units of C. trachomatis serovar E. Frozen sections were prepared from these tissues and were stained by immunohistochemical techniques. Infection with live, but not UV-inactivated, C. trachomatis induced a significant increase in levels of vascular cell adhesion molecule-1 and the mucosal addressin cell adhesion molecule-1 but not of other adhesion molecules. Therefore, infection with C. trachomatis induces adhesion molecules that are associated with other mucosal tissues and inflammatory sites, which suggests that mucosal routes of immunization may be effective.

ORIGINAL ARTICLE: The Combination of the Gastrointestinal Integrin (α4β7) and Selectin Ligand Enhances T‐Cell Migration to the Reproductive Tract During Infection with Chlamydia trachomatis

“…Previous in vitro studies revealing expression of adhesion molecules on human Fallopian tube tissue explants infected in vitro with Chlamydia trachomatis suggest that lymphocytes may use multiple adhesion pathways to migrate to human tissues6. We reported a significant upregulation of the mucosal adhesion molecule, MadCAM-1, and also a non-mucosal adhesion molecule associated with inflammation: vascular adhesion molecule-1, VCAM-1.…”

“…Investigation of murine and human systems have shown that CD4 T cells primed in lymphoid organs which drain mucosal sites increase surface expression of α4β7 integrin, also called the mucosal integrin; whereas those primed in lymph nodes draining peripheral or non-mucosal sites lose α4β7 integrin expression following antigen exposure and instead express P-selectin ligand and accumulate in peripheral tissues4, 5. The human female reproductive tract is a member of the common immune system and expresses the ligand for α4β7 integrin, MAdCAM-16. Thus, mucosal homing mechanisms are likely to control leukocyte entry into the GT.…”

ORIGINAL ARTICLE: Two Different Homing Pathways Involving Integrin β7 and E‐selectin Significantly Influence Trafficking of CD4 Cells to the Genital Tract Following Chlamydia muridarum Infection

“…Previous in vitro studies revealing expression of adhesion molecules on human Fallopian tube tissue explants infected in vitro with Chlamydia trachomatis suggest that lymphocytes may use multiple adhesion pathways to migrate to human tissues. 7 We reported a significant upregulation of the mucosal adhesion molecule, MadCAM-1, and also a non-mucosal adhesion molecule associated with inflammation: vascular adhesion molecule-1, VCAM-1. We also noted the marked increase of additional non-mucosal adhesion molecules; P-selectin and intracellular adhesion molecule-1 (ICAM-1).…”

“…We have previously reported that the mucosal adhesion molecule MadCAM and E & P-selectin are increased in the fallopian tube upon infection using the in vitro fallopian tube infection model 7. Although the murine analog which mediates the binding of lymphocytes to E-selectin has not yet been identified, in humans CLA binds to E-selectin.…”

Sex Hormones Selectively Impact the Endocervical Mucosal Microenvironment: Implications for HIV Transmission

“…In fact, about half of the CD4 + memory T cells in the FRT express various levels of integrin α 4 β 7 (Fig S1), Expression of α 4 β 7 marks immune cells that preferentially traffic to the gut lamina propria (LP) and associated lymphoid tissues (GALT) [15], [16]. However, α 4 β 7 high memory CD4 + T cells can also participate in immune responses in the FRT [17]–[19]. It is noteworthy that α 4 β 7 high CD4 + T cells are highly susceptible to HIV infection and are preferentially infected during the acute phase of SIV infection [20]–[22].…”