• 1 January 1980
    • journal article
    • research article
    • Vol. 41  (3) , 497-504
Abstract
Histamine produced dose-dependent inhibition of the production of the [human] 2nd complement component (C2) by monocytes in tissue culture. The effect was not associated with cell death, as ascertained by trypan blue exclusion, or loss of cells from the monolayer, as determined by measuring their DNA content. The specificity of the response was shown by the failure of histidine or histamine metabolites to inhibit C2 production. Preincubation of histamine with histaminase abrogated the histamine effect. The kinetics of the effect were extremely rapid and irreversible, most of the reduction being achieved during a 5 min exposure to histamine. The H2 [histamine] receptor antagonist cimetidine prevented the histamine response; chlorpheniramine, the H1 receptor antagonist, had no effect. Dimaprit and 4-methyl histamine, H2 receptor agonists, simulated the effect of histamine; the H1 receptor agonist 2-(2-amino-ethylthiazole) was ineffective, confirming that the effect of histamine on C2 production by monocytes is mediated by the H2 receptors. Histamine, released from basophils or mast cells by the C3 and C5 cleavage products C3a and C5a, respectively, may exert a negative feedback on further C3 and C5 cleavage by limiting the formation of the C3 .**GRAPHIC**. and C5 .**GRAPHIC**. convertases.