Influenza A virus potentiates basophil histamine release caused by endotoxin-induced complement activation. Examination of normal individuals and patients with intrinsic asthma.
Histamine release from human basophil leukocytes was triggered by complement activation by means of endotoxins isolated from E. coli and Salmonella bacteria. Influenza A virus was found to enhance the mediator release, and the effect was caused by synergism, since virus itself did not release histamine. The potentiating effect was similar in cells from normal individuals and from patients with intrinsic asthma. The involvement of viral neuraminidase was examined by a potent neuraminidase inhibitor and this inhibitor completely abolished the potentiating effect by virus. A purified neuraminidase preparation obtained from Vibrio cholerae caused a similar potentiating effect in mediator release and the effect was abolished by the neuraminidase inhibitor. These findings indicate that viral neuraminidase is responsible for the potentiating effect of virus on the histamine release. This effect might play a role in septic conditions and possibly contribute to asthmatic attacks by infections.
D000368:Aged; D003167:Complement Activation / Q000187:drug effects*; D004305:Dose-Response Relationship, Drug; D004731:Endotoxins / Q000494:pharmacology*; D006636:Histamine Release / Q000187:drug effects*; D006801:Humans; D009980:Influenza A virus / Q000502:physiology*; D008407:Mast Cells / Q000378:metabolism* / Q000503:physiopathology; D008875:Middle Aged; D009439:Neuraminidase / Q000037:antagonists & inhibitors; D012794:Sialic Acids / Q000494:pharmacology
D004731:Endotoxins; D012794:Sialic Acids; D009439:Neuraminidase