Proinflammatory potential of the airway epithelium in bronchial asthma

Raeburn, David; Webber, S. E.

doi:10.1183/09031936.94.07122226

Cited by 66 publications

(45 citation statements)

References 79 publications

(152 reference statements)

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“…In asthma, airway remodelling is described as increased thickening of the airway wall due to various structural alterations including: abnormal epithelium [50][51][52], sub-basement membrane thickening [53], alterations in interstitial matrix [54,55], increased vascularisation [56], alterations in mucous glands or enhanced mucus production [6], and an increase in smooth muscle mass [57]. These alterations are thought to have profound physiological consequences and are thought to be the consequence of the chronic inflammatory response that develops during the disease.…”

Section: Asm Remodelling: a Cause Of Asthma?mentioning

confidence: 99%

Treating asthma means treating airway smooth muscle cells

Zuyderduyn

Sukkar²,

Fust³

et al. 2008

Eur Respir J

123

113

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Asthma is characterised by airway hyperresponsiveness, airway inflammation and airway remodelling. Airway smooth muscle cells are known to be the main effector cells of airway narrowing. In the present paper, studies will be discussed that have led to a novel view of the role of airway smooth muscle in the pathogenesis of asthma in which airway hyperresponsiveness, remodelling and inflammation are, at least in part, attributable to airway smooth muscle. Furthermore, how this new view may lead to a change in the phenotyping and treatment of patients with asthma will be discussed.

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Section: Asm Remodelling: a Cause Of Asthma?mentioning

confidence: 99%

Treating asthma means treating airway smooth muscle cells

Zuyderduyn

Sukkar²,

Fust³

et al. 2008

Eur Respir J

123

113

View full text Add to dashboard Cite

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“…During this allergic response, epithelial cells play a significant role not only as a physical and biochemical barrier but also as a major source of cytokines, chemokines, and growth factors [2]. RANTES, IL-1, IL-6, and MCPs are known to be produced by bronchial epithelial cells [3]. We have also reported that eotaxin induced IL-8 and GM-CSF production from bronchial epithelial cells through CC chemokine receptor-3 (CCR3) [4].…”

Section: Introductionmentioning

confidence: 99%

Prostaglandin D<sub>2</sub> Induces IL-8 and GM-CSF by Bronchial Epithelial Cells in a CRTH2-Independent Pathway

Chiba

Kanda

Ueki

et al. 2006

Int Arch Allergy Immunol

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Background: Prostaglandin D₂ (PGD₂), a major prostanoid produced by activated mast cells, has long been implicated in allergic diseases. PGD₂ demonstrates its effects through two G-protein-coupled receptors, DP and CRTH2. The PGD₂/CRTH2 system mediates chemotaxis of eosinophils, basophils, and Th2 cells, which are involved in the induction of allergic inflammation. Although recent studies have shown that the specific receptors for PGD₂, DP, and CRTH2 are expressed in various human tissues, the role of PGD₂ is unknown in human bronchial epithelial cells. In this study, we investigated the expression and function of CRTH2/DP on NCI-H₂₉₂ and NHBE cells. Method: The CRTH2/DP expression was examined by RT-PCR and flow-cytometric analysis. NCI-H₂₉₂ and NHBE cells were cultured in the presence of various stimulants. The resulting supernatants were measured by ELISA. Results: We demonstrated that PGD₂ induced production of IL-8 and GM-CSF in NCI-H₂₉₂ and NHBE cells. DK-PGD₂ (CRTH2 agonist) and latanoprost (FP, a prostaglandin F receptor, agonist) failed to augment the production of these cytokines. Pretreatment with ramatroban (CRTH2 antagonist) and AL8810 (FP antagonist) did not reduce the production of these cytokines. The PGD₂-induced cytokine production was inhibited by pertussis toxin or specific inhibitors for MAP/ERK kinase (PD98059) and p38 MAP kinase (SB202190). Conclusion: These results suggest that PGD₂ is a potent inducer of IL-8 and GM-CSF production with MAP/ERK and p38 MAP kinase activation, but this is independent of CRTH2 activation.

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“…OH. Inhaled oxidants damage epithelial cells [23,24], and this may result in a loss of prostanoid inhibitory factors [25]. Oxidation of unsaturated fatty acids would result in an increased concentration of prostaglandins (PGE 2 ), which could also influence airway smooth muscle tone [23,25].…”

Section: Discussionmentioning

confidence: 99%

Acute exposure to hair bleach causes airway hyperresponsiveness in a rabbit model

Mensing

Marek²,

Raulf‐Heimsoth³

et al. 1998

Eur Respir J

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Ammonium persulphate (APS) and hydrogen peroxide (H2O2) are used as oxidants in many industrial processes and are the main constituents of standard hair bleaching products. In a previous study, it was demonstrated that aerosols of APS induce alterations in airway responsiveness. The present study examined whether exposure for 4 h to a hair bleach composition (containing APS, potassium persulphate and H2O2) or H2O2 could induce airway hyperresponsiveness and/or an obstructive ventilation pattern in a rabbit model. Exposure to the aerosols altered neither baseline airway resistance, dynamic elastance, slope of inspiratory pressure generation nor arterial blood pressure and blood gas measurements. Similarly to APS, hair bleach aerosols containing > or =10.9 mg x m(-3) persulphate (ammonium and potassium salt) in air and > or =1.36 mg x m(-3) H2O2 in air caused airway hyperresponsiveness to acetylcholine after 4 h of exposure. Aerosolized H2O2 (> or =37 mg x m(-3) in air) did not influence airway responsiveness to acetylcholine. The results demonstrate that hair bleaching products containing persulphates dissolved in H2O2 cause airway hyperresponsiveness to acetylcholine in rabbits.

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Proinflammatory potential of the airway epithelium in bronchial asthma

Cited by 66 publications

References 79 publications

Treating asthma means treating airway smooth muscle cells

Treating asthma means treating airway smooth muscle cells

Prostaglandin D<sub>2</sub> Induces IL-8 and GM-CSF by Bronchial Epithelial Cells in a CRTH2-Independent Pathway

Acute exposure to hair bleach causes airway hyperresponsiveness in a rabbit model

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