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Related Experiment Videos

The plasma contact system in atopic asthma.

E C Lasser, J H Lang, J G Curd

    The Journal of Allergy and Clinical Immunology
    |July 1, 1983
    PubMed
    Summary

    Atopic asthma patients show higher prekallikrein activation rates in plasma compared to controls. This suggests a link between contact system activation and atopy, with elevated endogenous heparin levels also observed in asthma patients.

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    Inflammation·2013

    Area of Science:

    • Biochemistry
    • Immunology
    • Hematology

    Background:

    • The contact system, involving prekallikrein activation, plays a role in inflammatory processes.
    • Atopic asthma is a complex inflammatory airway disease with poorly understood molecular mechanisms.
    • Dextran sulfate is known to activate the contact system in vitro.

    Purpose of the Study:

    • To investigate the rate of kallikrein appearance in plasma as a marker of contact system activation.
    • To compare contact system activation rates between individuals with atopic asthma and healthy controls.
    • To explore potential differences in endogenous heparin levels between the groups.

    Main Methods:

    • An in vitro assay was utilized to measure the rate of kallikrein appearance in plasma.

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  • Plasma samples were obtained from 19 patients with atopic asthma and 19 age- and sex-matched healthy controls.
  • Dextran sulfate was used to activate the contact system at 0°C.

    • Main Results:

    • The average prekallikrein activation rate was significantly higher in the plasma of atopic asthma patients compared to controls.
    • Elevated mean endogenous heparin levels were observed in the atopic asthma patient group.
    • These findings indicate heightened contact system activation in individuals with atopic asthma.

    Conclusions:

    • Contact system activation, as measured by prekallikrein activation rate, is increased in patients with atopic asthma.
    • Elevated endogenous heparin levels may be associated with atopic asthma.
    • These results suggest a potential role for the contact system in the pathophysiology of atopic asthma.