Premium
Preferential binding of Chlamydia trachomatis to subsets of human lymphocytes and induction of interleukin‐6 and interferon‐gamma
Author(s) -
FITZPATRICK D. R.,
WIE J.,
WEBB D.,
BONFIGLIOLI R.,
GARDNER I. D.,
MATHEWS J. D.,
BIELEFELDTOHMANN H.
Publication year - 1991
Publication title -
immunology and cell biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.999
H-Index - 104
eISSN - 1440-1711
pISSN - 0818-9641
DOI - 10.1038/icb.1991.49
Subject(s) - chlamydia trachomatis , biology , cytokine , population , cd8 , immunology , flow cytometry , peripheral blood mononuclear cell , interferon gamma , microbiology and biotechnology , interferon , antigen , in vitro , medicine , biochemistry , environmental health
Summary The interactions between Chlamydia trachumatis and human blood mononuclear leukocytes were studied using flow cytometry. Immunofluorescence, electron microscopy and cytokine assays. Under serum‐free conditions, elementary bodies (EB) of C. trachomatis were found to bind to human T lymphocytes as well as to B cells and monocytes/macrophages (Mφ). For all cell types the binding was saturable. rapid, temperature‐independent and independent of the chlamydia‐specific serological status of the donor. Similar proportions of T and B cells bound EB at similar levels. In the T cell population, proportionally less CD8 + cells bound EB. Whereas Mφ phagocytosed and destroyed the bound micro‐organisms for lymphocytes, the Chlamydia remained at the surface, adherent to morphologically featureless membrane areas and showed no evidence of uptake even after long periods at 37°C. Host molecules modulated these basic binding patterns: a heat‐stable serum factor inhibited EB binding to T cells and a heat‐labile serum factor enhanced binding to B cells. Stimulation with C. trachomatis EB rapidly elicited cytokine production by lymphocytes including interleukin‐6 from B cells and interferon‐gamma (IFN‐γ) from T and/or nonT/nonB cells. The responses were irrespective of the serological status of the donor. The findings suggest that C. trachomati‐leucocyte interactions may differ from the interactions of other bacteria and human leucocytes. The possible relationship between leucocyte‐binding, cytokine induction, and the pathognomonic development of lymphoid follicles during mucosal C. trachomatis infections is discussed.