Effect of interleukin-1β on airway hyperresponsiveness and inflammation in sensitized and nonsensitized Brown-Norway rats

Tsukagoshi, Hideo; Sakamoto, Tatsuo; Xu, Wenbin; Barnes, Peter J.; Chung, Kian Fan

doi:10.1016/0091-6749(94)90355-7

Cited by 58 publications

(34 citation statements)

References 16 publications

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“…Allergen challenge studies have also established that BK plays a pivotal role in the initiation of chronic airway inflammation (37). B2 BK receptor antagonists effectively block the development of the late-phase airway response as well as the development of bronchial hyperresponsiveness following allergen challenge in a number of different experimental animal models (3,4). To explore the mechanism by which BK promotes airway inflammation, we examined the ability of BK to regulate COX-2 expression in airway epithelial cells.…”

Section: Discussionmentioning

confidence: 99%

“…The release of BK is known to mediate multiple proinflammatory effects including smooth muscle contraction, vasodilation, increased vascular permeability, eicosanoid synthesis, and neuropeptide release (1,2). Furthermore, BK has been shown to play a critical role in the development of airway hyperresponsiveness in experimental models of airway inflammation (3)(4)(5). To elucidate the role of BK in this process, we assessed the effect of BK on cyclooxygenase-2 (COX-2) expression in human airway epithelial cells.…”

mentioning

confidence: 99%

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Bradykinin B2 Receptor Mediates NF-κB Activation and Cyclooxygenase-2 Expression via the Ras/Raf-1/ERK Pathway in Human Airway Epithelial Cells

Chen

Yu²,

Lei³

et al. 2004

The Journal of Immunology

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In this study, we investigated the signaling pathways involved in bradykinin (BK)-induced NF-κB activation and cyclooxygenase-2 (COX-2) expression in human airway epithelial cells (A549). BK caused concentration- and time-dependent increase in COX-2 expression, which was attenuated by a selective B2 BK receptor antagonist (HOE140), a Ras inhibitor (manumycin A), a Raf-1 inhibitor (GW 5074), a MEK inhibitor (PD 098059), an NF-κB inhibitor (pyrrolidine dithiocarbate), and an IκB protease inhibitor (l-1-tosylamido-2-phenylethyl chloromethyl ketone). The B1 BK receptor antagonist (Lys-(Leu8)des-Arg9-BK) had no effect on COX-2 induction by BK. BK-induced increase in COX-2-luciferase activity was inhibited by cells transfected with the κB site deletion of COX-2 construct. BK-induced Ras activation was inhibited by manumycin A. Raf-1 phosphorylation at Ser338 by BK was inhibited by manumycin A and GW 5074. BK-induced ERK activation was inhibited by HOE140, manumycin A, GW 5074, and PD 098059. Stimulation of cells with BK activated IκB kinase αβ (IKKαβ), IκBα phosphorylation, IκBα degradation, p65 and p50 translocation from the cytosol to the nucleus, the formation of an NF-κB-specific DNA-protein complex, and κB-luciferase activity. BK-mediated increase in IKKαβ activity and formation of the NF-κB-specific DNA-protein complex were inhibited by HOE140, a Ras dominant-negative mutant (RasN17), manumycin A, GW 5074, and PD 098059. Our results demonstrated for the first time that BK, acting through B2 BK receptor, induces activation of the Ras/Raf-1/ERK pathway, which in turn initiates IKKαβ and NF-κB activation, and ultimately induces COX-2 expression in human airway epithelial cell line (A549).

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Bradykinin B2 Receptor Mediates NF-κB Activation and Cyclooxygenase-2 Expression via the Ras/Raf-1/ERK Pathway in Human Airway Epithelial Cells

Chen

Yu²,

Lei³

et al. 2004

The Journal of Immunology

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“…Among them, interleukin (IL)-1β is notable [6][7][8] and has been described as inducing airway hyperresponsiveness. Indeed, intratracheal administration of IL-1β has been shown to induce airway hyperresponsiveness to bradykinin in rats [9].…”

Section: In Vitro-induced Human Airway Hyperresponsiveness To Bradykininmentioning

confidence: 99%

“…Among them, interleukin (IL)-1β is notable [6-8] and has been described as inducing airway hyperresponsiveness. Indeed, intratracheal administration of IL-1β has been shown to induce airway hyperresponsiveness to bradykinin in rats [9].Bradykinin has been implicated in the pathophysiology of asthma [10]. Inhaled bradykinin is a potent bronchoconstrictor in asthmatic patients, but is almost ineffective in normal subjects [11].…”

mentioning

confidence: 99%

In vitro-induced human airway hyperresponsiveness to bradykinin

Molimard¹,

Naline²,

Boichot³

et al. 1998

Eur Respir J

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aaAirway inflammation is one of the main features of asthma. It has been well established that people with respiratory infections may experience increased bronchial reactivity and impaired bronchial airflow [1,2]. Inhalation of endotoxin or lipopolysaccharide (LPS), a component of the outer cell wall of Gram-negative bacteria, has been reported to induce airway hyperresponsiveness in both normal [3] and asthmatic subjects [4]. The pathophysiological mechanisms underlying these changes after administration of LPS to the airways are not fully understood. Effects of LPS are likely to be indirect, through the activation of various inflammatory cells [5] which release the different endogenous inflammatory mediators and cytokines responsible for the host response. Among them, interleukin (IL)-1β is notable [6-8] and has been described as inducing airway hyperresponsiveness. Indeed, intratracheal administration of IL-1β has been shown to induce airway hyperresponsiveness to bradykinin in rats [9].Bradykinin has been implicated in the pathophysiology of asthma [10]. Inhaled bradykinin is a potent bronchoconstrictor in asthmatic patients, but is almost ineffective in normal subjects [11]. This feature may explain a key mechanism in the occurrence of airway hyperresponsiveness, which is a pathological characteristic of asthma.It has been established that bradykinin-induced human isolated bronchi contraction is linked to bradykinin B 2 receptor stimulation and subsequent prostanoid release [12][13][14]. The purpose of this study was to determine whether LPS and thereafter IL-1β induce hyperresponsiveness to bradykinin on human bronchial tissue in vitro and, if so, to analyse the mechanism of this hyperresponsiveness. Materials and methods Human bronchial tissue preparationBronchial tissues were removed from 22 patients (mean age 63 yrs, range 49-79 yrs) with lung cancer at the time of the surgical procedure. All were previous smokers. None were asthmatic. Just after resection, segments of bronchi with an inner diameter of 0.5-1 mm were taken from as far away as possible from the malignancy. They were placed in oxygenated Krebs-Henseleit solution (NaCl 119 mM, KCl 5.4 mM, CaCl 2 2.5 mM, KH 2 PO 4 0.6 mM, MgSO 4 1.2 mM, NaHCO 3 25 mM, glucose 11.7 mM) and stored overnight at 4°C. After removal of adhering fat and connective tissues, four to eight rings of the same bronchus were prepared. Each set of bronchial rings was suspended under an initial tension of 1.5 g in a 5 mL organ bath containing Krebs-Henseleit solution, bubbled with 95% O 2 /5% CO 2 and maintained at 37°C. The tissue was allowed to equilibrate over 1 h, during which time the KrebsHenseleit solution was changed every 15 min. Changes in LPS (100 ng·mL -1 for 3-6 h) and IL-1β (3×10 -10 and 3×10 -9 M for 20 min to 3 h) time-dependently potentiated bradykinin-induced contraction. This contraction was abolished, as in control experiments, by indomethacin (10 -6 M) or by the thromboxane (Tx) receptor antagonist GR 32191 but not by the cyclo-oxygenase-2 inhibitor, CG...

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“…Previous studies reported that interleukin (IL)-1b induces AHR in several animal models [11][12][13]. In addition, BARCHASZ et al [14] described that IL1b causes AHR to the NK-1 tachykinin receptor agonist [Sar 9 ,Met(O 2 ) 11 ]-substance P (SP) in the human isolated bronchus.…”

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confidence: 99%

Nerve growth factor is released by IL-1 and induces hyperresponsiveness of the human isolated bronchus

Frossard¹

2005

European Respiratory Journal

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Nerve growth factor (NGF) is a neurotrophic factor essential for the development and survival of neurons, and is also an important mediator of inflammation. It is released by airway cells stimulated by interleukin (IL)-1b. As IL-1b induces airway hyperresponsiveness (AHR) to the tachykinin NK-1 receptor agonist [Sar 9 ,Met(O 2 ) 11 ]-substance P in human isolated bronchi, the aim of this study was to determine whether IL-1b was able to induce NGF release from isolated bronchi, and whether NGF might participate into IL-1b-induced AHR.IL-1b (10 ng?mL -1 ; 21˚C; 15 h) increased the release of NGF from human isolated bronchi in vitro, and, in organ bath studies, the response of human bronchi to [Sar 9 ,Met(O 2 ) 11 ]-substance P (0.1 mm). A significant correlation was found between these responses. AHR induced by IL-1b was abolished by a blocking anti-human NGF antibody. Finally, NGF (1 ng?mL -1 ; 37˚C; 0.5 h) by itself induced a significant increase in [Sar 9 ,Met(O 2 ) 11 ]-substance P responsiveness. By contrast, it did not change the maximal contraction to acetylcholine.In conclusion, the present study clearly demonstrated that nerve growth factor may participate in the airway hyperresponsiveness induced by interleukin-1b, which supports the neuro-immune cross-talk that may be active in the development of hyperresponsiveness in the human airways, and suggests nerve growth factor is active in the airways in asthma.

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Effect of interleukin-1β on airway hyperresponsiveness and inflammation in sensitized and nonsensitized Brown-Norway rats

Cited by 58 publications

References 16 publications

Bradykinin B2 Receptor Mediates NF-κB Activation and Cyclooxygenase-2 Expression via the Ras/Raf-1/ERK Pathway in Human Airway Epithelial Cells

Bradykinin B2 Receptor Mediates NF-κB Activation and Cyclooxygenase-2 Expression via the Ras/Raf-1/ERK Pathway in Human Airway Epithelial Cells

In vitro-induced human airway hyperresponsiveness to bradykinin

Nerve growth factor is released by IL-1 and induces hyperresponsiveness of the human isolated bronchus

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