Pathogenesis of trachoma: the stimulus for inflammation.

Abstract

Abstract Active trachoma is characterized by chronic inflammation of the conjunctiva, and repeated episodes of reinfection are thought to be necessary to sustain this inflammation. It is currently believed that much of the tissue damage is immunologically mediated. To identify which antigens might be responsible for stimulating this continued inflammation, cynomolgus monkeys that had recovered from a previous ocular infection with Chlamydia trachomatis were challenged with various antigen preparations. Purified preparations of formalin- or UV-inactivated elementary bodies did not elicit any inflammation even with daily inoculation. In addition, neither purified chlamydial major outer membrane protein nor lipopolysaccharide, including recombinant organisms expressing the lipopolysaccharide group antigen, elicit inflammation. A soluble triton extract of the organism rapidly induced marked inflammation when inoculated in the eyes of immune monkeys but had no effect in naive animals. These studies suggest that the continual inflammation in trachoma may not be due to repeated exposure to chlamydial surface antigen(s) but rather to a labile product released by the living organisms.