Bradykinin stimulates interleukin‐8 production by human lung fibroblasts

Hayashi, Ryuji; Yamashita, Naohiro; Matsui, Shoko; Maruyama, Muneharu; Sugiyama, Eiji; Sugiyama, Shigeki; Kobayashi, Masashi

doi:10.1046/j.1365-2567.1998.00649.x

Cited by 18 publications

(18 citation statements)

References 27 publications

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“…It has previously been shown that BK stimulated human lung fibroblasts to produce IL-8 by increasing its gene expression [11]. In the present study, it has been further demonstrated that BK at nM concentrations stimulated human lung fibroblasts to produce IL-6 and IL-8 in a dose-and time-dependent manner.…”

Section: Discussionsupporting

confidence: 76%

“…Since the B2 receptor is a member of G protein-coupled receptor family, several steps are involved in the signal transduction leading to MAPK activation [30]. The authors recently reported that the stimulatory effect of BK on IL-8 production by lung fibroblasts is mediated, at least in part, via the PKC dependent pathway [11]. It has been reported that ERK 1/ 2 are enhanced via the PKC activation [31].…”

Section: Discussionmentioning

confidence: 99%

“…Normal parts of the tissue were washed with PBS, and pleural tissue and bronchi were removed after resection. Primary cultures of human lung fibroblasts were prepared as described elsewhere [19] with a few modifications [11]. Briefly, specimens were cut into small pieces and digested with 0.5±1 mg .…”

Section: Cell Preparation and Culturementioning

confidence: 99%

“…Total cellular ribonucleic acid (RNA) in the treated cells was extracted by acid guanidium thiocyanate-phenol-chloroform method using ISOGEN (Nippon Gene, Tokyo, Japan), and Northern blot analysis was carried out as previously described [11,20]. Twenty micrograms of total RNA was size-fractionated by electrophoresis through 1% agarose/17% formaldehyde gels, and transferred to nylon membranes (Ammersham, Oakville, Canada).…”

Section: Northern Blot Analysismentioning

confidence: 99%

“…Lung fibroblasts have the potential to induce inflammation in the alveolar interstitium by releasing proinflammatory cytokines in response to a variety of stimuli [8±10]. 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].…”

mentioning

confidence: 99%

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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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Section: Discussionsupporting

confidence: 76%

Section: Discussionmentioning

confidence: 99%

Section: Cell Preparation and Culturementioning

confidence: 99%

Section: Northern Blot Analysismentioning

confidence: 99%

mentioning

confidence: 99%

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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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Knee osteoarthritis: a role for bradykinin?

Meini

Maggi

2008

Inflamm. res.

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Osteoarthritis (OA) is a painful and degenerating progressive disease of the joints which affects millions of patients worldwide. The cause of OA is largely unknown. Among the potential therapies for the symptomatic treatment of OA, the intra-articular administration of a specific bradykinin (BK) B2 receptor antagonist has been reported to produce a long lasting analgesic effect in patients affected by knee OA. BK is a vasodilator and inflammatory nonapeptide which is generated in OA synovium. It contributes to the initiation and maintenance of inflammation, to exciting and sensitizing sensory nerve fibres, thus producing pain, and to activating synoviocytes and chondrocytes which are the main cells involved in the homeostasis of synovial fluid and cartilage, respectively. Moreover, BK synergistically potentiates the effects produced by pro-inflammatory cytokines. Biochemical and preclinical evidence supporting the therapeutic relevance of B2 receptor blockade in OA pathophysiology are reviewed in this publication.

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Transcriptomic analysis of lung development in wildtype and CFTR−/− sheep suggests an early inflammatory signature in the CF distal lung

Kerschner

Paranjapye

Schacht

et al. 2023

Funct Integr Genomics

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The precise molecular events initiating human lung disease are often poorly characterized. Investigating prenatal events that may underlie lung disease in later life is challenging in man, but insights from the well-characterized sheep model of lung development are valuable. Here, we determine the transcriptomic signature of lung development in wild-type sheep (WT) and use a sheep model of cystic fibrosis (CF) to characterize disease associated changes in gene expression through the pseudoglandular, canalicular, saccular, and alveolar stages of lung growth and differentiation. Using gene ontology process enrichment analysis of differentially expressed genes at each developmental time point, we define changes in biological processes (BP) in proximal and distal lung from WT or CF animals. We also compare divergent BP in WT and CF animals at each time point. Next, we establish the developmental profile of key genes encoding components of ion transport and innate immunity that are pivotal in CF lung disease and validate transcriptomic data by RT-qPCR. Consistent with the known pro-inflammatory phenotype of the CF lung after birth, we observe upregulation of inflammatory response processes in the CF sheep distal lung during the saccular stage of prenatal development. These data suggest early commencement of therapeutic regimens may be beneficial.

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Bradykinin stimulates interleukin‐8 production by human lung fibroblasts

Cited by 18 publications

References 27 publications

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

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

Knee osteoarthritis: a role for bradykinin?

Transcriptomic analysis of lung development in wildtype and CFTR−/− sheep suggests an early inflammatory signature in the CF distal lung

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