A Th1-type response develops following vaginal infection with the mouse pneumonitis biovar of Chlamydia trachomatis (MoPn). Since the type of response, i.e., Th1 versus Th2, can be influenced by factors present during T-cell activation, we examined the effects of different routes of MoPn administration on the cytokine profile and resistance against infection following a MoPn vaginal challenge. A dominant Th1-type cytokine profile developed in mice given live MoPn via the intranasal, oral, and vaginal routes with ratios of gamma interferon-secreting cells to interleukin 4-secreting cells greater than 10. In contrast, mice injected subcutaneously produced a Th2-type profile with a gamma interferon/interleukin 4 ratio of only 0.7. These mice also had significantly higher anti-MoPn immunoglobulin G1 serum titers, confirming a Th2-type cytokine profile. Exposure of mice to live MoPn, by any route prior to vaginal challenge, resulted in a shortened course of infection. However, the subcutaneous group resolved the vaginal infection more slowly, with 60% (6 of 10 mice) of the mice still isolation positive 12 days after challenge compared with only 20% of mice given live MoPn by other routes. Administration of UV-inactivated MoPn did not provide protection against a vaginal challenge. The decreased ability to clear infection was not associated with a shift in the cytokine profile, since intranasal and oral administration of UV-inactivated MoPn resulted in a predominant Th1-type response. Taken together, these data indicate that the initial route of MoPn administration can direct the type of response produced after a local MoPn infection and thus influence the ability of the immune response to protect against subsequent infection.
To evaluate the role of humoral immunity against simian immunodeficiency virus (SIV), we tested whether passive immunization with plasma from SIVmac251 vaccine-protected or healthy infected animals would protect rhesus monkeys against intravenous infection with ten 50% animal infectious doses of the cell-free homologous virus. The challenge dose of this SIVmac251 virus stock had previously caused persistent infection in all (21 of 21) nonimmunized controls. A plasma pool was obtained from a donor that had been immunized with an inactivated whole SIVmac251 vaccine produced in human T cells. This plasma pool contained low levels of SIVmac binding and neutralizing antibody but had a high titer of antibodies recognizing human cell proteins. Given 4 or 18 hr before intravenous challenge, this plasma completely protected three of eight recipients from infection and delayed virus detection in one recipient. The five unprotected animals had only a transient or undetectable p27 antigenemia and low virus load in their PBMCs, and all survived at least 7 months after infection. By contrast, no protection was observed in 6 monkeys given inactivated, pooled plasma or purified immunoglobulin (Ig) from healthy SIVmac251-infected animals. This plasma pool and the Ig preparation contained high levels of SIV-binding and neutralizing antibody but no reactivity to human cellular components. Five of the six recipients had persistent antigenemia after challenge and four died acutely from simian AIDS in 4-7 months. These studies suggest that passive transfer of antibody to human cellular antigens can confer protection against SIVmac whereas passive transfer of neutralizing antibodies without human cellular antibodies does not protect against the homologous virus and may enhance infection.
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