Activation of Kallikrein-Kinin System in Human Plasma with Purified Serine Protease from Dermatophagoides farinae

1990 ◽  
Vol 91 (1) ◽  
pp. 80-85 ◽  
Author(s):  
Katsunobu Takahashi ◽  
Takashi Aoki ◽  
Shoichi Kohmoto ◽  
Hiroyuki Nishimura ◽  
Yoh Kodera ◽  
...  
Keyword(s):  
Human Plasma ◽  
Serine Protease ◽  
Kinin System ◽  
Kallikrein Kinin System

scholarly journals Activation of the Kallikrein-Kinin System in Human Plasma by a Serine Protease from Mites.

1991 ◽  
Vol 10 (1) ◽  
pp. 15-20 ◽  
Author(s):  
Shoichi KOHMOTO ◽  
Yoh KODERA ◽  
Katsunobu TAKAHASHI ◽  
Hiroyuki NISHIMURA ◽  
Ayako MATSUSHIMA ◽  
...  
Keyword(s):  
Human Plasma ◽  
Serine Protease ◽  
Kinin System ◽  
Kallikrein Kinin System

Hereditary angioedema: Pathophysiology (HAE type I, HAE type II, and HAE nC1-INH)

2020 ◽  
Vol 41 (6) ◽  
pp. S14-S17 ◽  
Author(s):  
H. James Wedner
Keyword(s):  
Serine Protease ◽  
Hereditary Angioedema ◽  
Normal Activity ◽  
Genetic Alterations ◽  
Type I ◽  
Factor Xii ◽  
Kinin System ◽  
Major Pathway ◽  
Major Mechanism ◽  
Kallikrein Kinin System

The pathophysiology of hereditary angioedema (HAE) in virtually all cases is the result of the uncontrolled production of the vasoactive peptide bradykinin. C1 inhibitor (C1-INH) is a serine protease inhibitor, which, under normal circumstances, is the regulator of critical enzymes that are active in the cascades that result in bradykinin generation. In the classic forms of HAE, C1-INH is not produced in sufficient quantities (<40% of normal) or the function is <40% of normal activity. The major pathway for the production of bradykinin is the “contact system,” also known as the kallikrein-kinin system. This system begins with the activation of factor XII (FXII) to FXIIa, by a variety of physiologic and pathologic stimuli. FXIIa is a serine protease that binds to surfaces and cleaves prekallikrein to the active serine protease kallikrein. Kallikrein then cleaves high-molecular-weight kininogen to release the nonapeptide bradykinin. Bradykinin binds to the bradykinin β2 receptor, which increases vascular permeability and allows the flow of fluids into the extracellular space and results in angioedema. The two major enzymes generated in this cascade FXIIa and kallikrein are inhibited by C1-INH, which is the major regulator of this cascade. Failure to adequately control the production of bradykinin is thus the major mechanism for HAE. Several other types of HAE in which C1-INH is not decreased (HAE nlC1-INH) have been described. The alterations in FXII and plasminogen (also a serine protease inhibited by C1-INH) like with classic HAE are the result of dysregulation of bradykinin generation. Only genetic alterations in angiopoietin-1 may not be related to bradykinin generation, rather related to the control of the effect of bradykinin on the vascular endothelium.

scholarly journals Interaction of Bacteroides fragilis and Bacteroides thetaiotaomicron with the kallikrein–kinin system

Microbiology ◽  
2011 ◽  
Vol 157 (7) ◽  
pp. 2094-2105 ◽  
Author(s):  
Elizabeth C. Murphy ◽  
Matthias Mörgelin ◽  
Jakki C. Cooney ◽  
Inga-Maria Frick
Keyword(s):  
Human Plasma ◽  
Bacteroides Fragilis ◽  
Contact System ◽  
Opportunistic Pathogens ◽  
Bacteroides Thetaiotaomicron ◽  
Kinin System ◽  
Abdominal Abscesses ◽  
Significant Prolongation ◽  
Clotting Protein ◽  
Kallikrein Kinin System

Many bacterial pathogens interfere with the contact system (kallikrein–kinin system) in human plasma. Activation of this system has two consequences: cleavage of high-molecular-mass kininogen (HK) resulting in release of the potent proinflammatory peptide bradykinin, and initiation of the intrinsic pathway of coagulation. In this study, two species of the Gram-negative anaerobic commensal organism Bacteroides, namely Bacteroides fragilis and Bacteroides thetaiotaomicron, were found to bind HK and fibrinogen, the major clotting protein, from human plasma as shown by immunoelectron microscopy and Western blot analysis. In addition, these Bacteroides species were capable of activating the contact system at its surface leading to a significant prolongation of the intrinsic coagulation time and also to the release of bradykinin. Members of the genus Bacteroides have been known to act as opportunistic pathogens outside the gut, with B. fragilis being the most common isolate from clinical infections, such as intra-abdominal abscesses and bacteraemia. The present results thus provide more insight into how Bacteroides species cause infection.

Einfluss mechanischer Dehnung von alveolären Typ II Zellen auf das Kallikrein-Kinin System

Pneumologie ◽  
2016 ◽  
Vol 70 (S 01) ◽  
Author(s):  
J Knauth ◽  
A Schweinberger ◽  
H Kuhn ◽  
H Wirtz
Keyword(s):  
Kinin System ◽  
Kallikrein Kinin System
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