Interaction of paramyxoviruses with human basophils and their effect on histamine release.

We have demonstrated that human peripheral blood basophils released histamine on direct incubation with paramyxoviruses in vitro. Most histamine release occurred during the first 15 to 30 minutes after challenge, depending on the dose of virus used; release initiated by virus was complete by 1 hour. At a virus/cell ratio of 1:1, Sendai virus caused 41 +/- 9% histamine release, whereas parainfluenza type 3 (PI-3) virus caused 25 +/- 5% release and respiratory syncytial (RS) virus caused 19 +/- 5% release. Sendai, but not PI-3 or RS, also caused a decrease in cell number and release of lactic dehydrogenase; however, this apparent cell lysis did not account for all the histamine released. Incubation of cells with virus desensitized them to subsequent triggering by viruses but did not affect response of cells to other stimuli. Histamine release was dependent on the virus/cell ratio, temperature, and metabolic energy, but it was not strictly dependent on the presence of calcium in the extracellular medium. Histamine release was not affected by preincubation of cells with colchicine, suggesting that microtubules were not involved in the release process. Basophils desensitized by anti-IgE in the absence of calcium or treated with lactic acid to dissociate IgE molecules from membrane receptors released amounts of histamine similar to that of control basophils; thus, release was not initiated through Fc epsilon receptors. It was found, however, that histamine release by these viruses was greatly reduced when concanavalin A was used for desensitization. These data demonstrate that the respiratory viruses studied can cause direct nonimmunologic release of histamine from human basophils. Our findings provide evidence for another mechanism by which respiratory viruses can initiate inflammation.