Release of cytokines from isolated lung strips by bradykinin

Paegelow, I.; Werner, H.; Vietinghoff, Gabriele; Wartner, U

doi:10.1007/bf02032574

Cited by 34 publications

(27 citation statements)

References 30 publications

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“…However, little is known about the role of BK in regulating cytokine gene expression. A recent study demonstrated that BK stimulates the synthesis of IL-1␤, IL-2, and IL-6 from lung strip explants, an effect susceptible to blockade by a B2 BK receptor antagonist (31). Results presented in this report provide the first evidence that BK can stimulate cytokine gene expression through activation of the transcription factor NF-B, a potentially important mechanism for the inflammatory effects of kinins.…”

Section: Discussionmentioning

confidence: 52%

Bradykinin stimulates NF-kappaB activation and interleukin 1beta gene expression in cultured human fibroblasts.

et al. 1996

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Section: Discussionmentioning

confidence: 52%

Bradykinin stimulates NF-kappaB activation and interleukin 1beta gene expression in cultured human fibroblasts.

et al. 1996

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“…Bradykinin, kallidin, des-Arg 9 -bradykinin, des-Arg 10 -kallidin, NFormyl-Met-Leu-Phe (FMLP), leukotriene B 4 (LTB 4 …”

Section: Methodsmentioning

confidence: 99%

“…Paegelow/Trzeczak/Böckmann/Vietinghoff Additionally, kinins have themselves the capacity to induce the release or formation of further inflammatory mediators, for instance cytokines, prostaglandins and leukotrienes [3][4][5][6].…”

Section: Introductionmentioning

confidence: 99%

Migratory Responses of Polymorphonuclear Leukocytes to Kinin Peptides

Paegelow¹,

Trzeczak²,

Böckmann³

et al. 2002

Pharmacology

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The present study examines the influence of kinins on the migratory capacity of human polymorphonuclear leukocytes under in vitro conditions using the Boyden chamber technique. By means of checkerboard analysis the migration of neutrophils induced by bradykinin could be characterized as true chemotaxis. The stimulation of human neutrophils with bradykinin, with the nonpeptide B₂ receptor agonist FR190997 as well as with des-Arg⁹-bradykinin and des-Arg¹⁰-kallidin results in a concentration-dependent migration. Pretreatment of the neutrophils with the B₂ receptor antagonist HOE-140 (icatibant) inhibited the bradykinin-induced migration but not that induced by B₁ receptor agonists, whereas the B₁receptor antagonist des-Arg¹⁰HOE-140 abolished the migration elicited by des-Arg⁹-bradykinin or des-Arg¹⁰-kallidin but not that evoked by bradykinin. Pretreatment of the neutrophils with the leukotriene B₄ (LTB₄) antagonist ZK158252 inhibited the LTB₄-induced chemotaxis as well as the chemotaxis produced by bradykinin and des-Arg¹⁰-kallidin. An involvement of interleukin-1β and of the chemokine IL-8 in the bradykinin-induced migration in vitro could be excluded during the migration time of the neutrophils. In conclusion, the present study provides pharmacological evidence showing that B₁ and B₂ kinin receptors are involved in the migration of human neutrophils in vitro, that LTB₄ participates in the downstream pathway and that the B₁ kinin receptor seems to be expressed already under physiological conditions.

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“…Recently, it has been reported that BK stimulated human lung fibroblasts to produce interleukin (IL)-8 by increasing its gene expression [11]. BK also increases the production of IL-1, IL-2, and IL-6 from isolated guinea pig lung strips [12], and IL-1 from cultured human lung fibroblasts [13]. These data suggest that BK may be involved in the control of the inflammatory reaction associated with interstitial lung disorders through proinflammatory cytokines production by lung fibroblasts.…”

mentioning

confidence: 99%

Bradykinin stimulates IL-6 and IL-8 production by human lung fibroblasts through ERK- and p38 MAPK-dependent mechanisms

Hayashi¹,

Yamashita

Matsui

et al. 2000

Eur Respir J

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Bradykinin (BK) is a major kinin with well-documented pharmacological properties including vascular leakage and induction of a variety of cytokines. However, the intracellular signalling mechanisms by which BK induced proinflammatory cytokine production have not been fully elucidated. This study investigated the role of the extracellular signal-regulated protein kinase 1/2 (ERK 1/2) and p38 mitogen-activated protein kinase (p38 MAPK) in the BK-induced interleukin (IL)-6 and IL-8 production by human lung fibroblasts.Lung fibroblasts were stimulated with BK in the presence or in the absence of PD98059, a specific MAPK/ERK kinase-1 inhibitor, or SB203580, a specific p38 MAPK inhibitor, and IL-6 or IL-8 production and their gene expression was examined. BK-induced ERK 1/2 or p38 MAPK phosphorylation was also analysed by Western blot analysis.BK at nanomolar concentrations stimulated lung fibroblasts to produce IL-6 and IL-8 along with increased ERK 1/2 and p38 MAPK phosphorylation. BK-induced IL-6 and IL-8 synthesis was inhibited by a B2-type BK receptor antagonist. Furthermore, PD98059 or SB203580 significantly suppressed BK-induced IL-6 and IL-8 production and their gene expression.These results indicate that bradykinin-induced interleukin-6 and interleukin-8 production are at least partly mediated through the extracellular signal-related protein kinase 1/2 and p38 mitogen-activated protein kinase pathway-dependent activation in human lung fibroblasts, and suggest that bradykinin appears to be involved in the inflammatory reaction leading to acute lung injury through stimulating interleukin-6 and interleukin-8 production by lung fibroblasts. Eur Respir J 2000; 16: 452±458.

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Release of cytokines from isolated lung strips by bradykinin

Cited by 34 publications

References 30 publications

Bradykinin stimulates NF-kappaB activation and interleukin 1beta gene expression in cultured human fibroblasts.

Bradykinin stimulates NF-kappaB activation and interleukin 1beta gene expression in cultured human fibroblasts.

Migratory Responses of Polymorphonuclear Leukocytes to Kinin Peptides

Bradykinin stimulates IL-6 and IL-8 production by human lung fibroblasts through ERK- and p38 MAPK-dependent mechanisms

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