Effect of histamine on the gene expression and biosynthesis of complement components C2, factor B and C3 in mouse

Immunology
|April 1, 1987
PubMed

Insights

Histamine affects complement component production in mouse macrophages. It inhibits C2 and factor B via H2 receptors, while C3 is modulated by both H1 and H2 receptors, indicating pretranslational control.

Area of Science:

  • Immunology
  • Pharmacology

Background:

  • Histamine is a key mediator in immune responses.
  • Complement system components like C2, factor B, and C3 are crucial for innate immunity.
  • Macrophages play a central role in immune regulation.

Purpose of the Study:

  • To investigate the in vitro effects of histamine on the gene expression and biosynthesis of complement components C2, factor B, and C3 in mouse peritoneal macrophages.
  • To determine the histamine receptor subtypes (H1 and H2) involved in regulating these complement components.

Main Methods:

  • Incubation of mouse resident peritoneal macrophages with varying concentrations of histamine.
  • Quantification of C2, factor B, and C3 mRNA levels using specific assays.
  • Assessment of protein levels through immunoprecipitation.
  • Use of H1 and H2 receptor antagonists and agonists to elucidate receptor involvement.

Main Results:

  • Histamine significantly decreased C2 and factor B mRNA and protein levels, an effect mediated primarily through H2 receptors.
  • C3 gene expression and biosynthesis were influenced by both H1 and H2 receptors, with differential effects observed.
  • The regulation of these complement components by histamine appears to occur at the pretranslational level.

Conclusions:

  • Histamine differentially regulates complement component biosynthesis in mouse macrophages.
  • C2 and factor B regulation is predominantly H2 receptor-dependent.
  • C3 regulation involves both H1 and H2 receptors, suggesting complex histamine signaling pathways in macrophage-mediated immunity.

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