Chlamydia trachomatis (CT) antibody-mediated opsonophagocytosis is not associated with reduced endometrial or incident infection.

Authors

Bryce W Duncan, Jiahao Zhang, Celeste R Robles, Kacy S Yount, Xiaojing Zheng, Catherine M O'Connell, Toni Darville

Published in

The Journal of infectious diseases. Oct 08, 2026. Epub Oct 08, 2026.

Abstract

Naturally acquired antibodies to Chlamydia trachomatis (CT) are associated with reduced cervical bacterial burden but not with protection from endometrial or subsequent CT infection. We investigated whether antibody-mediated opsonophagocytosis, a functional measure of humoral immunity, was associated with protection against these clinical outcomes.
Serum samples from 139 women enrolled in the longitudinal T cell Response Against Chlamydia (TRAC) cohort and 11 healthy seronegative controls were evaluated for Fc receptor-mediated opsonophagocytosis of CellTrace Violet-labeled CT elementary bodies using THP-1 monocytes. Associations with anti-chlamydial antibody titers, cervical bacterial burden, endometrial infection, and incident CT infection during 12 months of follow-up were assessed.
Opsonophagocytic activity correlated strongly with anti-chlamydial antibody titers and was significantly higher in seropositive women than in seronegative controls. Although a weak inverse correlation with cervical bacterial burden was observed, neither the proportion of phagocytic cells nor the extent of bacterial uptake was associated with reduced endometrial infection. Similarly, neither measure differed between women who experienced incident CT infection during follow-up and those who remained infection-free.
Naturally acquired anti-chlamydial antibodies promoted Fc receptor-mediated uptake of CT; however, antibody-mediated opsonophagocytic activity was not associated with protection from endometrial or subsequent CT infection. These findings suggest that naturally acquired antibody-mediated opsonophagocytic activity is unlikely to serve as a correlate of protection against CT infection.

PMID:
42848926
Bibliographic data and abstract were imported from PubMed on 09 Oct 2026.

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