Kyle H Ramsey1, Namir Shaba, Kevin P Cohoon, Kevin A Ault. 1. Department of Microbiology, Chicago College of Osteopathic Medicine, Midwestern University, Downers Grove, IL 60515, USA. kramse@midwestern.edu
Abstract
OBJECTIVE: We postulated that either oral or vaginal administration of the immune response modifier imiquimod would decrease vaginal shedding of Chlamydia trachomatis, mouse pneumonitis strain (MoPn), in a murine model. METHODS: Female BALB/c mice were infected intravaginally with C. trachomatis (MoPn) and were administered imiquimod either orally (30 mg/kg) or vaginally (10 microl of 5% imiquimod cream) prior to infection and every second day after infection for a total of four doses. The course of infection was monitored by collecting cervical-vaginal swabs and isolation in HeLa 229 cell culture. To determine whether the drug affected T helper type 1 or T helper type 2 immune response polarization, immunoglobulin G (IgG) subclass antibody responses were assessed at day 56 after infection. RESULTS: There was no significant difference in the course of infection when imiquimod-treated mice were compared with sham-treated controls, regardless of whether the drug was administered orally or vaginally. IgG subclass antibody responses, and by extension, T helper type 1 to T helper type 2 immune response polarization, were also unaffected. CONCLUSIONS: Imiquimod has no efficacy in controlling C. trachomatis (MoPn) infection in the murine model.
OBJECTIVE: We postulated that either oral or vaginal administration of the immune response modifier imiquimod would decrease vaginal shedding of Chlamydia trachomatis, mousepneumonitis strain (MoPn), in a murine model. METHODS: Female BALB/c mice were infected intravaginally with C. trachomatis (MoPn) and were administered imiquimod either orally (30 mg/kg) or vaginally (10 microl of 5% imiquimod cream) prior to infection and every second day after infection for a total of four doses. The course of infection was monitored by collecting cervical-vaginal swabs and isolation in HeLa 229 cell culture. To determine whether the drug affected T helper type 1 or T helper type 2 immune response polarization, immunoglobulin G (IgG) subclass antibody responses were assessed at day 56 after infection. RESULTS: There was no significant difference in the course of infection when imiquimod-treated mice were compared with sham-treated controls, regardless of whether the drug was administered orally or vaginally. IgG subclass antibody responses, and by extension, T helper type 1 to T helper type 2 immune response polarization, were also unaffected. CONCLUSIONS: Imiquimod has no efficacy in controlling C. trachomatis (MoPn) infection in the murine model.