ABSTRACT
Incubation of human leukocytes with certain viruses results in the enhancement of IgE-mediated release of histamine. This enhancement is produced by interferon. The present experiments show that an induction period of 6 to 9 hr and new RNA synthesis are required for interferon to enhance histamine release. This points to the possibility that interferon may exert its antiviral and histamine-release enhancing activities by acting through a common pathway.
Subject(s)
Basophils/metabolism , Histamine Release , Immunoglobulin E , Interferons/pharmacology , RNA/biosynthesis , Allergens , Antibodies, Anti-Idiotypic , Dactinomycin/pharmacology , Humans , Time FactorsSubject(s)
Adenosine Triphosphatases/metabolism , Escherichia coli/metabolism , Methylglucosides/metabolism , Methylglycosides/metabolism , Arabinose/pharmacology , Biological Transport , Calcium/pharmacology , Carbonyl Cyanide m-Chlorophenyl Hydrazone/pharmacology , Enzyme Activation/drug effects , Escherichia coli/drug effects , Kinetics , Magnesium/pharmacology , Mutation , Oxygen Consumption/drug effects , Species Specificity , Succinates/pharmacologyABSTRACT
The uptake of methyl alpha-D-glucopyranoside (alpha-MG) by Escherichia coli K12 was decreased by the addition of substrates which stimulated the rate of oxygen consumption by the cells. The inhibition, which occurred only at non-saturating concentrations of alpha-MG, was not the result of a stimulation of the rate of exit of intracellular alpha-MG, and was abolished by the presence of carbonyl cyanide m-chlorophenylhydrazone or sodium azide. Since those drugs inhibit energy conservation at the respiratory chain and did not alter significantly the rate of oxygen consumption under the conditions for the assay of alpha-MG uptake, it appears that the inhibition of the transport system by respirable substrates is mediated by some form of energy derived from respiration.
