title: Production of colony-stimulating factors during pneumonia caused by Chlamydia trachomatis.
abstract: The colony-stimulating factors (CSFs) are cytokines involved in the production, differentiation, and activation of host phagocytes. During murine infection with Chlamydia trachomatis (MoPn), plasma CSF levels increased in euthymic (nu/+) and athymic (nu/nu) BALB/c mice. Levels declined later in infection, with the nu/+ mice resolving the infection but the nu/nu mice succumbing by day 16. Either live or heat-killed Chlamydia organisms could induce CSF increases on day 7 postchallenge in nu/+ mice; however, by day 14, only mice challenged with live organisms maintained high plasma levels. CSFs were also produced by spleen cells of nu/+ and nu/nu mice in response to Chlamydia antigen. Spleen cell CSF production was detectable by days 3 to 5 postinfection. In nu/+ mice, spleen cell CSF production was elevated throughout the rest of the time course but in nu/nu mice fell significantly at day 14. Like the plasma CSF activity (CSA) production, spleen cell CSA production on day 7 was seen in mice challenged with either live or heat-killed Chlamydia organisms, but on day 14 only nu/+ mice challenged with live organisms maintained significant CSA production. To further characterize the T-cell dependence of CSA production, spleen cells of nu/+ mice were depleted of T cells or T-cell subsets before producing supernatants. On day 14 postinfection, the CD4+ lymphocyte was the major producer of CSFs. Additionally, there were different types of CSFs secreted by nu/+ and nu/nu mice as determined by the ability of spleen cell supernatants to support the granulocyte-macrophage CSF/interleukin 3-dependent cell line FDCP-1. Supernatants from nu/+ mice had 4 to 8 times the level of FDCP-1 CSF activity of the supernatants from nu/nu mice. These results support the evidence that nu/+ mice were producing some CSFs by T-cell-dependent mechanisms. This is the first report of CSF production in vivo during Chlamydia infection. Furthermore, we show that CSFs are produced by both T-cell-dependent and T-cell-independent mechanisms. The capacity of the CSFs to increase the production and effector function of phagocytes may be important to host defenses.
authors.affiliation: Department of Medicine, University of Texas Health Science Center, San Antonio.
authors.forename: D M
authors.initials: DM
authors.lastname: Magee
authors.forename: D M
authors.initials: DM
authors.lastname: Williams
authors.forename: E J
authors.initials: EJ
authors.lastname: Wing
authors.forename: C A
authors.initials: CA
authors.lastname: Bleicker
authors.forename: J
authors.initials: J
authors.lastname: Schachter
mesh_terms: D000818:Animals; D002690:Chlamydia Infections / Q000503:physiopathology*; D002692:Chlamydia trachomatis / Q000276:immunology*; D003115:Colony-Stimulating Factors / Q000096:biosynthesis*; D005260:Female; D016178:Granulocyte-Macrophage Colony-Stimulating Factor / Q000096:biosynthesis; D007377:Interleukin-3 / Q000096:biosynthesis; D008297:Male; D051379:Mice; D008819:Mice, Nude; D011014:Pneumonia / Q000503:physiopathology*; D013047:Specific Pathogen-Free Organisms; D013154:Spleen / Q000503:physiopathology; D013601:T-Lymphocytes / Q000276:immunology; D013997:Time Factors
chemical_list: D003115:Colony-Stimulating Factors; D007377:Interleukin-3; D016178:Granulocyte-Macrophage Colony-Stimulating Factor