Please use this identifier to cite or link to this item: http://repositorio.unifesp.br/handle/11600/26466
Title: Altered neutrophil homeostasis in kinin B1 receptor-deficient mice
Authors: Araujo, R. C.
Kettritz, R.
Fichtner, I
Paiva, ACM
Pesquero, J. B.
Bader, M.
Universidade Federal de São Paulo (UNIFESP)
Max Delbruck Ctr Mol Med
Keywords: B1 receptor
bradykinin
gene targeting
immune system
inflammation
leukocytes
Issue Date: 1-Jan-2001
Publisher: Walter de Gruyter & Co
Citation: Biological Chemistry. Berlin: Walter de Gruyter & Co, v. 382, n. 1, p. 91-95, 2001.
Abstract: The kallikrein-kinin system is activated during inflammation and plays a major role in the inflammatory process. One of the main mechanisms of kinin action includes the modulation of neutrophil function employing both receptors for kinins, B1 and B2, in this report we show by the use of B1 receptor-deficient mice that neutrophil migration in inflamed tissues is dependent on kinin B1 receptors, However, there is no change in circulating leukocyte number and composition after genetic ablation of this receptor. Furthermore, apoptosis of neutrophils necessary for the resolution of persistent inflammatory processes is impaired in mice lacking the B1 receptor. We also show that this receptor is expressed on neutrophils, thus it may be directly involved in the induction of apoptosis in these cells after prolonged activation at inflamed sites. in conclusion, our data show that the kinin B1 receptor modulates migration and the life span of neutrophils at sites of inflammation and may be therefore an important drug target in the therapy of inflammatory diseases.
URI: http://repositorio.unifesp.br/handle/11600/26466
ISSN: 1431-6730
Other Identifiers: http://dx.doi.org/10.1515/BC.2001.014
Appears in Collections:Em verificação - Geral

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