Inflammation Kallikreins

Clements J. The molecular biology of the kallikreins and their roles in inflammation. In Farmer S, editor. The Kinin System. New York Academic Press, 1997 71-97. 

Bhoola K, Ramsaroop R, Plendl J, Cassim B, Dlamini Z, Naicker S. Kallikrein and kinin receptor expression in inflammation and cancer. Biol Chem 2001 382 77-89. 

Its mechanism of action, however, is not completely elucidated. Kamakura et aL [94] studied the effects of stem bromelain on tlw plasma kallikrein system, bradykinin levels and plasma exudation at the inflammatory site in rats with a kaolin-induced inflammation of an air couch. Bromelain caused a dose-... 

The anti-inflaminatory action of bromelain preparations is the result of dif-fjrjnt mechanisms thatnft simultaneous 11. First there is, as described sbevr, the depletion of the plasma kallikrein system, inhibiting the generation of bndykinin, a known chemical mediator of inflammation. Second, there is a negative action... 

Muscle cells release kallikrein during inflammation causing formation of active kinin peptides (bradykinin and kallidin) from kininogen [65, 66]. Kinins are peptide hormones that produce vasodilation, increase capillary permeability, and cause pain and infiltration of neutrophils. There is a direct correlation between the amount of kinin in plasma or tissues and the degree of inflammation. Vascular dilation causes increased blood flow to infection [67, 68], Bik inhibits formation of kinins and vascular dilation by kallikrein, thereby inhibiting smooth muscle contraction [69-71],... 

Inflammation leads to vasodilation that damages the endothelial and epithelial layers, thus promoting vascular disease [4], Kallikrein, neutrophil elastase, and mast cell tryptase release kinins from kininogens. Kinins are... 

Bik decreases ischemia/reperfusion injury by inhibiting proteases that cause kinin release [4, 99]. Reversion to a normal blood pressure occurs in two ways through inhibition of kallikrein with protease inhibitors and by destruction of kinins by kinase. Bik decreases kinin formation through their effect on kallikrein. The duration of kinin formation and destruction ranges from 2 to 30 min [100, 101]. After 30 min, little kinin activity is detectable. As inflammation abates, so does neutrophil chemotaxis and endothelial adherence to the basement membrane. PAR also regulates vascular tone and participates in response to vascular injury. Bik inhibits PAR activation [79, 80],... 

The kinin-kallikrein system (kinin system) is a poorly delineated system of blood proteins that plays a role in inflammation, blood-pressure control, coagulation and pain. Kinins are small peptides produced from kininogen by kallikrein, which are subsequently degraded by kininases. They act on phospholipase and increase arachidonic acid release and thus prostaglandin (PGE2) production. 

Thi ,DPhe BK [Thi ,DPhe ]-bradykinin. bradykinin-potentiating peptide teprotide. bradykinin potentiator B teprotide. BRADYKININ RECEPTOR AGONISTS act at sites recognizing members and derivatives of the bradykinin family of hormone peptides - kinins - of which bradykinin (BK) and kallidin (lysyl-bradykinin Lys-BK KD) are the main mammalian members. The bradykinin family is distinct from the tachykinin family of peptides, though both have profound hypotensive actions and contract many intestinal and other smooth muscles. Historically, it was noted that the former action was relatively slow-developing, hence the name bradykinin. Notable actions of bradykinin and kallidin are to dilate blood vessels and increase their permeability to plasma proteins, and to stimulate sensory nerve C-fibres. These actions are pro-inflammatory, and reflect the fact that the kinin-formation system is activated in inflammation, and enzymes (kallikreins) form the kinins from blood-borne or tissue precursors (kininogens) on injurious insult. 

Its mechanism of action, however, is not completely elucidated. Kamakura et al. [94] studied the effects of stem bromelain on the plasma kallikrein system, bradykinin levels and plasma exudation at the inflammatory site in rats with a kaolin-induced inflammation of an air pouch. Bromelain caused a dose-dependent decrease of bradykinin levels (measured with the method of Minami et al. [95]) at the inflammatory site and a parallel decrease of the prekallikrein levels in sera [88]. Plasma exudation was also reduced dose-dependently. Bradykinin-degrading activity in sera was elevated after bromelain treatment, but not in the pouch fluid. The authors conclude that bromelain inhibits plasma exudation through inhibition of the bradykinin generation at the inflammatory site via depletion of the plasma kallikrein system. Bromelain also shows a dose-dependent analgesic effect in concanavalin A-injected paws of 5.6 mg/kg i.v.), considered to be due to decrease of high molecular weight kininogen [96]. 

KInIns, human peptide hormones implicated in many physiological and pathological processes, including reduction of blood pressure and regulation of sodium homeostasis, inflammation and the cardioprotective effects of preconditioning. The kallikrein-kinin system (KKS) of the plasma generates bradykinin (BK), whereas the tissue KKS is responsible for the formation of kallidin. The kinin action is mediated via two types of kinin receptor, the type 1 (Bi) and type 2 (B2). Bi... 

The role of platelet activation in initiation and propagation of coagulation is well studied. More recently, it has been demonstrated that activated platelets serve as a hub in thromboinflammation, in that they are linked to activation of the complement system by various mechanisms as well as to activation of the contact/kallikrein system. In both cases, these interactions lead to enhanced inflammation, suggesting that the platelet functions as an innate immune cell [7]. 

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