Induction of arthritis in C57B1/6 mice by chlamydial antigen. Effect of prior immunization or infection.

Abstract

Antigen from a Chlamydia trachomatis biovar, mouse pneumonitis agent (MoPn), was used to produce an inflammatory arthritis by inoculation in the knee joints of C57B1/6 mice. The production of arthritis was strongly dependent on prior sensitization to chlamydiae by subcutaneous immunization in either sex or genital infection in females. In unimmunized animals quantitatively less inflammation, fibrin exudation, and pannus formation developed than in immunized counterparts. In neither uninjected nor McCoy or HeLa Cell antigen-treated joints did arthritis develop. The arthritis produced was more pronounced at 7 than at 2 days after intraarticular challenge and showed minimal residual changes at 21 days. Residual changes included subsynovial hyperplasia. In genitally infected female mice less severe arthropathy developed than in subcutaneously immunized female mice after intraarticular challenge with formalin-inactivated chlamydial antigen. However, in infected mice challenged with chlamydiae inactivated by ultraviolet irradiation a severe arthritis with destructive pannus developed, suggesting alteration of antigenicity by formalin inactivation. The strong association of the arthritis with the presence of chlamydial antibody suggests its use as a model of human Reiter's disease in which prior sensitization to Chlamydia is an important factor.

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