Virus enhances IgE- and non-IgE-dependent histamine release induced by bacteria and other stimulators.
Histamine release from human basophil leukocytes was triggered by Staph. aureus, Salmonella enteritidis, non-haemolytic streptococci, or E. coli. Influenza A virus was found to enhance the mediator release and the effect was caused by synergism, since the virus did not induce release of histamine per se. This potentiating effect of the virus was seen both when the bacteria-induced histamine release was IgE-dependent (i.e. patient sensitized to the bacterium) and when the bacterium caused mediator release by a non-immunological mechanism independent of IgE (putative sugar-lectin mediated). Histamine release induced by anti-IgE and calcium ionophore or agarose-beads was also enhanced in the presence of the virus. These findings indicate that influenza A virus potentiates both IgE- and non-IgE-mediated histamine release induced by bacteria and other stimulators.
Clementsen
P
P
Department of Pharmacology, University of Copenhagen, Denmark.
Pedersen
M
M
Permin
H
H
Espersen
F
F
Jarløv
J O
JO
Norn
S
S
D001424:Bacterial Infections / Q000378:metabolism*; D001491:Basophils / Q000187:drug effects / Q000378:metabolism*; D000001:Calcimycin / Q000494:pharmacology; D004927:Escherichia coli Infections / Q000378:metabolism; D006636:Histamine Release / Q000187:drug effects*; D006801:Humans; D007073:Immunoglobulin E / Q000276:immunology*; D066298:In Vitro Techniques; D009980:Influenza A virus / Q000276:immunology; D012480:Salmonella Infections / Q000378:metabolism; D013203:Staphylococcal Infections / Q000378:metabolism; D013290:Streptococcal Infections / Q000378:metabolism
D007073:Immunoglobulin E; D000001:Calcimycin