Clementsen P, Jensen C B, Jarløv J O, Hannoun C, Norn S
Department of Pharmacology, University of Copenhagen, Denmark.
Agents Actions. 1988 Apr;23(3-4):165-7. doi: 10.1007/BF02142529.
Histamine release from human basophil leukocytes was triggered by Staph. aureus or by complement activation caused by endotoxins isolated from E. coli or Salmonella bacteria. Influenza A virus was found to enhance the mediator release and the effect was caused by synergism, since the virus itself did not release histamine. The potentiating effect of the virus was abolished by a potent neuraminidase inhibitor. Furthermore, a purified neuraminidase preparation obtained from Vibrio cholerae caused a similar potentiating effect, which was also abolished by the neuraminidase inhibitor. These findings indicate that the neuraminidase on the surface of influenza A virus is responsible for the potentiating effect of the virus on basophil histamine release.
金黄色葡萄球菌或从大肠杆菌或沙门氏菌中分离出的内毒素所引起的补体激活可触发人嗜碱性粒细胞释放组胺。发现甲型流感病毒可增强介质释放,且这种作用是由协同作用引起的,因为病毒本身并不释放组胺。一种强效神经氨酸酶抑制剂可消除病毒的增强作用。此外,从霍乱弧菌中获得的纯化神经氨酸酶制剂也会产生类似的增强作用,且同样会被神经氨酸酶抑制剂所消除。这些发现表明,甲型流感病毒表面的神经氨酸酶是该病毒对嗜碱性粒细胞组胺释放产生增强作用的原因。