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Virus enhances IgE- and non-IgE-dependent histamine release induced by bacteria and other stimulators
P Clementsen1, M Pedersen, H Permin
1Department of Pharmacology, University of Copenhagen, Denmark.
Abstract:
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.
Insights
Influenza A virus enhances histamine release from human basophils, triggered by bacteria or other stimuli. This potentiation occurs through synergistic effects, impacting both IgE-dependent and IgE-independent pathways.
Area of Science:
- Immunology
- Virology
- Cell Biology
Background:
- Human basophil leukocytes play a crucial role in immune responses through histamine release.
- Bacterial infections and viral infections can independently influence immune cell activity.
- Histamine release can be mediated by both immunoglobulin E (IgE)-dependent and IgE-independent mechanisms.
Purpose of the Study:
- To investigate the effect of Influenza A virus on histamine release from human basophils.
- To determine if Influenza A virus potentiates histamine release induced by bacterial stimuli.
- To elucidate the mechanisms underlying the virus-induced enhancement of histamine release.
Main Methods:
- Incubation of human basophil leukocytes with various bacterial species (Staph. aureus, Salmonella enteritidis, E. coli, non-haemolytic streptococci).
- Co-incubation of basophils with Influenza A virus and bacterial stimuli.
- Assessment of histamine release using IgE-dependent and IgE-independent stimulation methods (e.g., anti-IgE, calcium ionophore, agarose beads).
Main Results:
- Influenza A virus synergistically enhanced histamine release triggered by multiple bacterial species.
- The virus potentiated histamine release irrespective of whether the bacterial stimulus was IgE-dependent or IgE-independent.
- Influenza A virus also enhanced histamine release induced by non-bacterial stimuli like anti-IgE, calcium ionophore, and agarose beads.
Conclusions:
- Influenza A virus significantly potentiates histamine release from human basophils.
- This potentiation effect is observed for both IgE-mediated and non-IgE-mediated histamine release pathways.
- The findings suggest a broader role for influenza A virus in modulating inflammatory responses beyond direct viral effects.