Immune Response Against Chlamydia trachomatis Inoculation in Mice

Changes of Interferon Activity, Antibody Titers and Weight of the Spleen as Parameters of Infection

Abstract

We examined the immune response against Chlamydia trachomatis (serovar L2) inoculation in mice by measuring the serum interferon (IFN) level, 2'-5'A synthetase (2-5A (S)) activity, antibody titers (IgM, IgG) and the spleen weight as parameters of infection. The interferon activity was detected 6 hrs (400 U/ml) and the activity peaked 12 hrs (450 U/ml) after inoculation, and then gradaully decreased thereafter (24 hrs: 12 U/ml, 36 hrs: undetectable). It was found that Chlamydia trachomatis induces IFN as well as bacteria. To monitor the behavior of IFN action after serum IFN was cleared, 2-5A (S) activity in the spleen cell extract was measured. It was found that the activity reached its peak 1 to 2 days after inoculation and then decreased as well as in infectivity of Chlamydia trachomatis. The activity however was almost not detected in sera of mice after inoculation of heat-inactivated Chlamydial organism (56°C, 10 min). This may indicate that intact Chlamydial organisms were required for induction of IFN. IFN induced in mice was stable in pH 2.0 treatment and IFN induced by Newcastle disease virus inhibited growth of Chlamydia trachomatis in L929 cell cultures in a dosedependent manner. The weight of the spleen gradually increased and reached its peak (2-to 3-fold of the control) in 3 to 5 days after inoculation, and then gradually decreased to the control level. IgM and IgG antibodies to Chlamydia trachomatis were detected by immunofluorescence method and enzyme-linked immunosorbent assay, respectively. The antibody IgM was detected as early as 2 days and reached its peak 3 to 4 days after inoculation. The antibody IgG was detected 7 days after inoculation and gradually increased thereafter.
The change of these parameters show host immune responses against Chlamydia trachomatis. We believe that these findings are useful for understanding the defence mechanism in Chlamydial infection.