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Chlamydia muridarum Major Outer Membrane Protein‐Specific Antibodies Inhibit In Vitro Infection but Enhance Pathology In Vivo
Author(s) -
Cunningham Kelly A.,
Carey Alison J.,
Hafner Louise,
Timms Peter,
Beagley Kenneth W.
Publication year - 2011
Publication title -
american journal of reproductive immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.071
H-Index - 97
eISSN - 1600-0897
pISSN - 1046-7408
DOI - 10.1111/j.1600-0897.2010.00894.x
Subject(s) - chlamydia , antibody , chlamydia trachomatis , immunology , immune system , biology , in vivo , sexually transmitted disease , immunity , chlamydiaceae , infertility , virology , pregnancy , genetics , microbiology and biotechnology , syphilis , human immunodeficiency virus (hiv)
Citation Cunningham KA, Carey AJ, Hafner L, Timms P, Beagley KW. Chlamydia muridarum major outer membrane protein‐specific antibodies inhibit in vitro infection but enhance pathology in vivo. Am J Reprod Immunol 2011; 65: 118–126 Problem Chlamydia trachomatis is a significant worldwide health problem, and the often‐asymptomatic disease can result in infertility. To develop a successful vaccine, a complete understanding of the immune response to chlamydial infection and development of genital tract pathology is required. Method of Study We utilized the murine genital model of chlamydial infection. Mice were immunized with chlamydial major outer membrane protein, and vaginal lavage was assessed for the presence of neutralizing antibodies. These samples were then pre‐incubated with Chlamydia muridarum and administered to the vaginal vaults of immune‐competent female BALB/c mice to determine the effect on infection. Results The administration of C. muridarum in conjunction with neutralizing antibodies reduced the numbers of mice infected, but a surprising finding was that this accelerated the development of severe oviduct pathology. Conclusion Antibodies play an under‐recognized role in chlamydial infection and pathology development, which possibly involves interaction with Th1 immunity.