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Kinin generation in acute pneumonia and chronic bronchitis
1Dept of Clinical Immunology and Asthma, Virchow-Klinikum, Humboldt University Berlin, Germany.
The European Respiratory Journal
|August 1, 1997
Summary
In acute airway inflammation, plasma kallikrein generates kinins, while chronic bronchitis involves other kininogenases like tissue kallikrein. This study differentiates kinin generation pathways in lower airway inflammatory conditions.
Area of Science:
- Biochemistry
- Immunology
- Pulmonology
Background:
- Kinins are key mediators in inflammatory processes.
- Understanding kinin generation is crucial for studying airway inflammation.
Purpose of the Study:
- To investigate kinin generation pathways in acute and chronic lower airway inflammation.
- To differentiate the roles of plasma kallikrein and tissue kallikrein in these conditions.
Main Methods:
- Analysis of bronchoalveolar lavage fluid (BALF) from patients with pneumonia, chronic bronchitis, and healthy controls.
- Quantification of kinins, plasma kallikrein (pl-Kal), alpha2-macroglobulin (alpha2-M), and toluenesulphonylarginine methyl ester (TAME) esterase activity (TAME-ea) using RIA, ELISA, and radiochemical assays.
- Gel filtration chromatography and inhibition tests to identify specific kallikreins involved.
Main Results:
- Plasma kallikrein and alpha2-M levels were significantly higher in acute pneumonia compared to chronic bronchitis.
- Gel filtration identified plasma kallikrein as the primary contributor to TAME-ea at ~800 kDa in acute pneumonia.
- Tissue kallikrein was identified as the main contributor to TAME-ea at ~40 kDa in chronic bronchitis.
Conclusions:
- Kinin generation in acute airway inflammation is predominantly mediated by plasma kallikrein.
- In chronic airway inflammation, kininogenases other than plasma kallikrein, notably tissue kallikrein, play a more significant role.