Zariffard M Reza, Harwani Sailesh, Novak Richard M, Graham Parrie J, Ji Xin, Spear Gregory T
Department of Immunology/Microbiology, Rush University, Chicago, IL 60612, USA.
Clin Immunol. 2004 Apr;111(1):103-7. doi: 10.1016/j.clim.2003.12.008.
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-alpha 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-alpha responses were not reduced by Polymyxin B and did not correlate with beta(2)-defensin levels, indicating that stimulation of cells was not through lipopolysaccharide or beta(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.
虽然阴道毛滴虫感染可导致炎症并使白细胞流入女性生殖道，但诱导这些效应的重要分子途径尚不清楚。本研究确定阴道毛滴虫感染是否通过Toll样受体4（TLR4）激活细胞。感染女性的生殖道分泌物可刺激具有功能性TLR4的细胞产生TNF-α（350 pg/ml），但对TLR4配体无反应的细胞产生的TNF-α显著较少（44 pg/ml，P = 0.001）。感染清除后收集的分泌物对具有功能性TLR4的细胞诱导的反应也显著降低（136 pg/ml，P = 0.008）。多粘菌素B未降低TNF-α反应，且与β2-防御素水平无关，表明细胞刺激不是通过脂多糖或β2-防御素。这些研究表明，阴道毛滴虫感染导致生殖道中出现通过TLR4刺激细胞的物质，提示了这种感染引起炎症的机制。
