Pfaff A W, Georges S, Candolfi E
Institut de Parasitologie et de Pathologie Tropicale, Interaction Cellulaire et Moléculaire Hôte-Parasite (E.A. 3950), Faculté de Médecine, Strasbourg, France.
Parasite Immunol. 2008 Sep;30(9):487-90. doi: 10.1111/j.1365-3024.2008.01047.x.
This study investigated the effect of infection with the apicomplexan parasite Toxoplasma gondii, in combination with the concomitant cytokine environment (IFN-gamma/TNF-alpha), on adhesion of THP-1 monocytic cells to MRC-5 fibroblasts. Surprisingly, infection of THP-1 cells decreased their adhesion to the MRC-5 cell monolayer. This decrease was compensated by IFN-gamma/TNF-alpha stimulation. In contrast, infection of MRC-5 cells significantly increased adhesion, which was synergistically augmented by cytokine stimulation. Levels of ICAM-1 (CD54) on MRC-5 cells, as well as LFA-1 (CD11a) on THP-1 cells, were not changed by infection, neither in resting, nor in cytokine stimulated cells. These results show that T. gondii infection alters adhesion properties and reactivity to cytokine stimulation in a cell-specific way.
本研究调查了顶复门寄生虫刚地弓形虫感染,结合伴随的细胞因子环境(IFN-γ/TNF-α),对THP-1单核细胞与MRC-5成纤维细胞黏附的影响。令人惊讶的是,THP-1细胞感染后降低了它们与MRC-5细胞单层的黏附。这种降低通过IFN-γ/TNF-α刺激得到补偿。相反,MRC-5细胞感染显著增加了黏附,细胞因子刺激使其协同增强。MRC-5细胞上ICAM-1(CD54)以及THP-1细胞上LFA-1(CD11a)的水平,在静息细胞或细胞因子刺激的细胞中,均未因感染而改变。这些结果表明,刚地弓形虫感染以细胞特异性方式改变黏附特性和对细胞因子刺激的反应性。