Trichomonas vaginalis infection activates cells through toll-like receptor 4

While Trichomonas vaginalis infection can cause inflammation and influx of leukocytes into the female genital tract, the molecular pathways important in inducing these effects are not known. This study determined if infection with T. vaginalis activates cells through toll-like receptor 4 (TLR4). Gen...

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Bibliographic Details
Published in:Clinical immunology (Orlando, Fla.) Fla.), 2004-04, Vol.111 (1), p.103-107
Main Authors: Zariffard, M.Reza, Harwani, Sailesh, Novak, Richard M, Graham, Parrie J, Ji, Xin, Spear, Gregory T
Format: Article
Language:English
Subjects:
Animals
beta-Defensins - immunology
Biological and medical sciences
Bodily Secretions
Cell Line
Female
Fundamental and applied biological sciences. Psychology
Fundamental immunology
Genital tract
Humans
Immunopathology
Leukocytes - immunology
Lipopolysaccharide, β 2-defensin
Medical sciences
Membrane Glycoproteins - immunology
Mice
Monocytes - immunology
Receptors, Cell Surface - immunology
Therapeutic Irrigation
TNF-α
Toll-like receptor
Toll-Like Receptor 4
Toll-Like Receptors
Trichomonas vaginalis
Trichomonas vaginalis - immunology
Trichomonas Vaginitis - immunology
Tumor Necrosis Factor-alpha - biosynthesis
Vagina - secretion
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Summary:While Trichomonas vaginalis infection can cause inflammation and influx of leukocytes into the female genital tract, the molecular pathways important in inducing these effects are not known. This study determined if infection with T. vaginalis activates cells through toll-like receptor 4 (TLR4). Genital tract secretions from infected women stimulated TNF-α production by cells with functional TLR4 (350 pg/ml) but significantly less by cells that are unresponsive to TLR4 ligands (44 pg/ml, P = 0.001). Secretions collected after clearance of infection also induced significantly lower responses by cells with functional TLR4 (136 pg/ml, P = 0.008). TNF-α responses were not reduced by Polymyxin B and did not correlate with β 2-defensin levels, indicating that stimulation of cells was not through lipopolysaccharide or β 2-defensin. These studies show that T. vaginalis infection results in the appearance in the genital tract of substance(s) that stimulate cells through TLR4, suggesting a mechanism for the inflammation caused by this infection.
ISSN:1521-6616
1521-7035
DOI:10.1016/j.clim.2003.12.008