Bradykinin- and lipopolysaccharide-induced bradykinin B2 receptor expression, interleukin 8 release and “nitrosative stress” in bronchial epithelial cells BEAS-2B: Role for neutrophils

Ricciardolo, Fabio Luigi Massimo; Sorbello, Valentina; Benedetto, Sabrina; Defilippi, Ilaria; Sabatini, Federica; Robotti, Andrea; Renswouw, Dein C. van; Bucca, Caterina; Folkerts, Gert; Rose, Virginia De

doi:10.1016/j.ejphar.2012.07.051

Cited by 11 publications

(9 citation statements)

References 40 publications

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“…In this study, an increase in IL-8, MPO and nitrosative stress, by means of 3-NT production, was evidenced in BEAS-2B cells cocultured with neutrophils compared to BEAS-2B cells alone reaching the maximal effect at 8 h of incubation, and LPS increased 3-NT release as we previously demonstrated [4]. Ambroxol and beclomethasone alone showed an inhibitory effect on LPS-induced IL-8 and MPO release and 3-NT formation in BEAS-2B cells cocultured with neutrophils, and the combination of the two drugs enhanced their effect on IL-8 and 3-NT.…”

Section: Discussionsupporting

confidence: 54%

“…In our previous study we showed that bradykinin and LPS-induced bradykinin B2 receptor expression and nitrosative stress through the IL-8 pathway in BEAS-2B cells co-incubated with neutrophils, suggesting a role for bradykinin, via neutrophil activation, in the formation of nitrosative stress [4]. Moreover, both human rhinoviruses and house dust mites upregulated IL-8 release in BEAS-2B cells, while RANTES release was induced only by human rhinoviruses [28].…”

Section: Discussionmentioning

confidence: 99%

“…Estimations of the percentages of non-viable cells were made by counting the percentage of blue cells. Viability values were on average higher than 98% [4]. …”

Section: Methodsmentioning

confidence: 99%

“…Immortalized, non-tumorigenic human bronchial epithelial cells BEAS-2B (CRL-9609; American Type Culture Collection, Manassas, Va., USA) were cultured in a serum-free medium composed of 50% LHC9 medium (Gibco, Grand Island, N.Y., USA) and 50% RPMI-1640 medium (Euroclone Ltd., Paignton, UK) supplemented with 1× non-essential amino acids (Gibco), L -glutamine (2 m M ), penicillin (100 U/ml)/streptomycin (100 U/ml; Euroclone Ltd.), and incubated at 37°C in 100% humidity and 5% CO 2 [4]. …”

Section: Methodsmentioning

confidence: 99%

“…Bradykinin and lipopolysaccharide (LPS) stimulate neutrophil chemo-attractant interleukin (IL)-8 release and production of 3-NT and MPO (a marker of neutrophil activation) by human bronchial epithelial (BEAS-2B) cells cultured alone or with human polymorphonuclear neutrophils (PMNs) [4]. Furthermore, epithelial cells release IL-8 and 3-NT after stimulation by viruses [5], nitrogen dioxide [6] and acute lung injury [7].…”

Section: Introductionmentioning

confidence: 99%

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Effect of Ambroxol and Beclomethasone on Lipopolysaccharide-Induced Nitrosative Stress in Bronchial Epithelial Cells

Ricciardolo¹,

Sorbello²,

Benedetto³

et al. 2015

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Background: Nitrosative stress is involved in different airway diseases. Lipopolysaccharide (LPS) induces neutrophil-related cytokine release and nitrosative stress in human bronchial epithelial (BEAS-2B) cells alone or with human polymorphonuclear neutrophils (PMNs). Ambroxol protects against oxidative stress, and beclomethasone dipropionate is an anti-inflammatory drug. Objectives: We evaluated the ability of ambroxol and/or beclomethasone dipropionate to inhibit LPS-induced expression/release of RANTES, IL-8, inducible NO synthase (iNOS), myeloperoxidase (MPO) and 3-nitrotyrosine (3-NT: nitrosative stress biomarker) in BEAS-2B ± PMNs stimulated with LPS (1 μg/ml). Methods: The effect of ambroxol and/or beclomethasone dipropionate on IL-8, RANTES and iNOS levels was assessed by Western blot analysis; IL-8, MPO and 3-NT levels were measured by ELISA. Cell viability was assessed by the trypan blue exclusion test. Results: In BEAS-2B alone, LPS (at 12 h) increased RANTES/iNOS expression and IL-8 levels (p < 0.001). Ambroxol suppressed LPS-induced RANTES expression and IL-8 release (p < 0.001), whilst inhibiting iNOS expression (p < 0.05). Beclomethasone dipropionate had no effect on RANTES but halved iNOS expression and IL-8 release. Coculture of BEAS-2B with PMNs stimulated IL-8, MPO and 3-NT production (p < 0.001), potentiated by LPS (p < 0.001). Ambroxol and beclomethasone dipropionate inhibited LPS-stimulated IL-8, MPO and 3-NT release (p < 0.05). Ambroxol/beclomethasone dipropionate combination potentiated the inhibition of IL-8 and 3-NT production in BEAS-2B with PMNs (p < 0.05 and p < 0.01, respectively). Ambroxol and/or beclomethasone dipropionate inhibited nitrosative stress and the release of neutrophilic inflammatory products in vitro. Conclusion: The additive effect of ambroxol and beclomethasone dipropionate on IL-8 and 3-NT inhibition suggests new therapeutic options in the treatment of neutrophil-related respiratory diseases such as chronic obstructive pulmonary disease and respiratory infections.

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Section: Discussionsupporting

confidence: 54%

Section: Discussionmentioning

confidence: 99%

“…Estimations of the percentages of non-viable cells were made by counting the percentage of blue cells. Viability values were on average higher than 98% [4]. …”

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Effect of Ambroxol and Beclomethasone on Lipopolysaccharide-Induced Nitrosative Stress in Bronchial Epithelial Cells

Ricciardolo¹,

Sorbello²,

Benedetto³

et al. 2015

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Bradykinin in asthma: Modulation of airway inflammation and remodelling

Ricciardolo

Folkerts

Folino

et al. 2018

European Journal of Pharmacology

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Bradykinin, a pro-inflammatory molecule, and its related peptides have been studied for their effects on acute reactions in upper and lower airways, where they can be synthesised and metabolized after exposure to different stimuli including allergens and viral infection. Bradykinin B and B receptors are constitutively expressed in the airways on several residential and/or immune cells. Their expression can also be induced by inflammatory mediators, usually associated with eosinophil and neutrophil recruitment, such as IL-4, IL-13, TNF-α, IL-6 and IL-8, via intracellular MAPK and NF-κB signalling. In turn, the latters up-regulate both bradykinin receptors. Bradykinin activates epithelial/endothelial and immune cells, neurons and mesenchymal cells (such as fibroblasts, myofibroblasts and smooth muscle cells), which are implicated in the development of airway chronic inflammation, responsiveness and remodelling (a major feature of severe asthma). This review highlights the role of bradykinin and its receptors in respect to chronic inflammatory response involving eosinophils/neutrophils and to vascular/matrix-related airway remodelling in asthmatic airways. This scenario is especially important for understanding the mechanisms involved in the pathogenesis of eosinophilic and/or neutrophilic asthma and hence their therapeutic approach.

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Protective effects of polydatin on lipopolysaccharide-induced acute lung injury through TLR4-MyD88-NF-κB pathway

Jiang

Guo

et al. 2015

International Immunopharmacology

169

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Bradykinin- and lipopolysaccharide-induced bradykinin B2 receptor expression, interleukin 8 release and “nitrosative stress” in bronchial epithelial cells BEAS-2B: Role for neutrophils

Cited by 11 publications

References 40 publications

Effect of Ambroxol and Beclomethasone on Lipopolysaccharide-Induced Nitrosative Stress in Bronchial Epithelial Cells

Effect of Ambroxol and Beclomethasone on Lipopolysaccharide-Induced Nitrosative Stress in Bronchial Epithelial Cells

Bradykinin in asthma: Modulation of airway inflammation and remodelling

Protective effects of polydatin on lipopolysaccharide-induced acute lung injury through TLR4-MyD88-NF-κB pathway

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