The intent of this research is to provide evidence that interferons and mononucler phagocytes can not only control Chlamydia psittaci replication, but also enhance the chronic or persistent state. To accomplish this long-term objective, we will study chlamydial persistence in both in vitro and in vivo models.
The specific aims of this project are to (1) determine whether interferon plays a regulatory role in chlamydial persistence in the mouse, and in a mouse fibroblast model, (2) document chlamydial replication or inhibition within cultured human monocytes (nonpermissive) and monocyte derived machrophages (permissive), ans study the mechanisms by which monocytes restrict chlamydial development, and (3) examine the capacity of resident (human alveolar) macrophages to support the growth of Chlamydia, as well as restrict its replication in response to interferon activation. Chlamydial development within host cells will be studied using conventional and fluorescent antibody stains, infectivity assays, and by electron microscopy. Identification of the factors that control chlamydial persistence may provide a basis for approaching the pharmacological or immunological management of patients with chronic chlamydial disease.
| Rothermel, C D; Schachter, J; Lavrich, P et al. (1989) Chlamydia trachomatis-induced production of interleukin-1 by human monocytes. Infect Immun 57:2705-11 |
| Rothermel, C D; Rubin, B Y; Jaffe, E A et al. (1986) Oxygen-independent inhibition of intracellular Chlamydia psittaci growth by human monocytes and interferon-gamma-activated macrophages. J Immunol 137:689-92 |
