Castellanos C, Ramos C, Ortiz-Ortiz L
Departamento de Immunología, Universidad Nacional Autónoma de México, Mexico City.
Infect Immun. 1989 Sep;57(9):2771-5. doi: 10.1128/iai.57.9.2771-2775.1989.
To define the participation of cell-mediated immunity in resistance to amebic infection through the action of soluble mediators or lymphokines (LKs), including gamma interferon (IFN-gamma), we studied their effect on Entamoeba histolytica. Supernatants from cultures of lymphoid cells, which had been stimulated in vitro with concanavalin A and were rich in lymphokines (LRSNs), and recombinant IFN-gamma were used. LRSN and recombinant IFN-gamma inhibited the growth of E. histolytica trophozoites in vitro. These LKs did not show a cytotoxic effect on the ameba, but they did inhibit rather significantly protein and DNA syntheses of the protozoa. Interestingly, LRSN incubated at 4 degrees C in the presence of trophozoites lost the ability to inhibit the replication of vesicular stomatitis virus. IFN-gamma inactivated at pH 2 had no effect on DNA synthesis by the ameba, thus suggesting that IFN-gamma is responsible for the observed inhibition of parasite growth. Furthermore, the IFN-gamma inhibitory effect was abolished by a monoclonal antibody specific for this LK. The results suggest that IFN-gamma may participate in protection against amebiasis infection through the activity of mediators released by lymphocytes during infection.
为了通过可溶性介质或淋巴因子(LKs)(包括γ干扰素(IFN-γ))的作用来确定细胞介导的免疫在抗阿米巴感染中的参与情况,我们研究了它们对溶组织内阿米巴的影响。使用了经伴刀豆球蛋白A体外刺激且富含淋巴因子的淋巴细胞培养上清液(LRSNs)以及重组IFN-γ。LRSN和重组IFN-γ在体外抑制了溶组织内阿米巴滋养体的生长。这些LKs对阿米巴没有显示出细胞毒性作用,但它们确实相当显著地抑制了原生动物的蛋白质和DNA合成。有趣的是,在滋养体存在的情况下于4℃孵育的LRSN失去了抑制水疱性口炎病毒复制的能力。在pH 2下失活的IFN-γ对阿米巴的DNA合成没有影响,因此表明IFN-γ是观察到的寄生虫生长抑制的原因。此外,针对该LK的单克隆抗体消除了IFN-γ的抑制作用。结果表明,IFN-γ可能通过感染期间淋巴细胞释放的介质的活性参与预防阿米巴病感染。