Inhaled corticosteroid reduced <i>lamina reticularis</i> of the basement membrane by modulation of insulin‐like growth factor (IGF)‐I expression in bronchial asthma

Hoshino, Makoto; Nakamura, Yutaka; Jj, Sim; Yamashiro, Yuichiro; Uchida, Kyoko; Hosaka, Kimio; Isogai, Sho

doi:10.1046/j.1365-2222.1998.00277.x

Cited by 126 publications

(91 citation statements)

References 51 publications

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“…The findings from these studies also suggest that the degree of fibrosis is related to AHR, consistent with past studies [30][31][32] that have shown that in addition to collagen IV being increased in the subepithelial layer various interstitial collagens are also synthesized and deposited into areas surrounding the subepithelial and within interstitial regions of the airway in human asthma. This increase in aberrant collagen deposition increases total wall thickness of the airway, resulting in a reduction in the diameter of the airway lumen.…”

Section: Discussionsupporting

confidence: 79%

Characterization of a novel model incorporating airway epithelial damage and related fibrosis to the pathogenesis of asthma

Royce

Patel

Samuel

2014

Laboratory Investigation

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Asthma develops from injury to the airways/lungs, stemming from airway inflammation (AI) and airway remodeling (AWR), both contributing to airway hyperresponsiveness (AHR). Airway epithelial damage has been identified as a new etiology of asthma but is not targeted by current treatments. Furthermore, it is poorly studied in currently used animal models of AI and AWR. Therefore, this study aimed to incorporate epithelial damage/repair with the well-established ovalbumin (OVA)-induced model of chronic allergic airway disease (AAD), which presents with AI, AWR, and AHR, mimicking several features of human asthma. A 3-day naphthalene (NA)-induced model of epithelial damage/repair was superimposed onto the 9-week OVA-induced model of chronic AAD, before 6 weeks of OVA nebulization (NA þ OVA group), during the second last OVA nebulization period (OVA/NA group) or 1 day after the 6-week OVA nebulization period (OVA þ NA group), using 6-8-week-old female Balb/c mice (n ¼ 6-12/group). Mice subjected to the 9-week OVA model, 3-day NA model or respective vehicle treatments (saline and corn oil) were used as appropriate controls. OVA alone significantly increased epithelial thickness and apoptosis, goblet cell metaplasia, TGF-b1, subepithelial collagen (assessed by morphometric analyses of various histological stains), total lung collagen (hydroxyproline analysis), and AHR (invasive plethysmography) compared with that in saline-treated mice (all Po0.05 vs saline treatment). NA alone caused a significant increase in epithelial denudation and apoptosis, TGF-b1, subepithelial, and total lung collagen compared with respective measurements from corn oil-treated controls (all Po0.01 vs corn oil treatment). All three combined models underwent varying degrees of epithelial damage and AWR, with the OVA þ NA model demonstrating the greatest increase in subepithelial/total lung collagen and AHR (all Po0.05 vs OVA alone or NA alone). These combined models of airway epithelial damage/AAD demonstrated that epithelial damage is a key contributor to AWR, fibrosis and related AHR, and augments the effects of AI on these parameters.

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Section: Discussionsupporting

confidence: 79%

Characterization of a novel model incorporating airway epithelial damage and related fibrosis to the pathogenesis of asthma

Royce

Patel

Samuel

2014

Laboratory Investigation

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“…In one study of 10 patients with severe asthma, despite longterm corticosteroid treatment (mean 3.7 yrs), the asthmatic subjects showed thickening of basement membrane reticular collagen comparable to controls without asthma [46]. In contrast, in 24 patients with asthma, 6 months of treatment with inhaled beclomethasone dipropionate, compared to placebo, decreased the number of activated eosinophils, T-cells and fibroblasts and the thickness of the lamina reticularis in biopsy samples from the bronchial mucosa [47]. In another bronchial bioptic study of 14 patients with asthma, 3 months of budesonide treatment (compared to baseline) reduced the number of infiltrating eosinophils and lymphocytes and improved the structure of the bronchial epithelium [48].…”

Section: Discussionmentioning

confidence: 99%

Increase in laminin expression in allergic airway remodelling and decrease by dexamethasone

Pe¹,

Jonas²,

Tsai³

et al. 2004

Eur Respir J

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Lung expression of the extracellular matrix protein, laminin, and its receptor, laminin-1 receptor, were examined in a mouse model of asthma with airway remodelling.Ovalbumin (OVA) was administered to BALB/c mice, intraperitoneally on days 0 and 14, and intranasally periodically between days 14 and 75.The mice developed airway eosinophil and mononuclear inflammatory cell infiltration and fibrosis. On day 76, a marked increase in total laminin was seen in the airways of OVA-treated mice compared to controls by Western blot analysis. The increased laminin expression was detected immunocytochemically in the thickened subepithelial basement membrane and around airways and blood vessels. The OVA-treated mice showed increased expression of the a1, b1, and c1 chains of the laminin-1 isoform in monocytes, macrophages and eosinophils infiltrating the airways. Laminin-1 receptor expression was increased in inflammatory and endothelial cells in the lungs of OVAtreated mice compared to controls. Treatment of OVA-sensitised/challenged mice with dexamethasone reduced airway expression of laminin and laminin-1 receptor in OVAtreated mice but not airway hyperresponsiveness to methacholine.Laminin deposition may be an important component of the airway remodelling observed in chronic allergic lung inflammation and is a process modulated by corticosteroids.

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“…IGF-I is a potent mitogen and stimulant of collagen secretion in fibroblasts (2), and has been implicated in the pathogenesis of fibrosis in a number of lung disorders (3)(4)(5). IGF-I is up-regulated in the airways of mice after allergen challenge (6), and IGF-I levels in biopsies of patients with asthma correlate with subepithelial fibrosis (7). The regulation of IGF-I is mediated, in part, by a system of six IGFBPs (8).…”

mentioning

confidence: 99%

Role of Insulin-like Growth Factor Binding Protein-3 in Allergic Airway Remodeling

Veraldi

Gibson

Yasuoka³

et al. 2009

Am J Respir Crit Care Med

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Inhaled corticosteroid reduced lamina reticularis of the basement membrane by modulation of insulin‐like growth factor (IGF)‐I expression in bronchial asthma

Abstract: These results suggest that corticosteroid treatment in asthma can reduce the lamina reticular thickness by modulation of IGF-I expression with consequent inhibition of the airway infiltration by inflammatory cells, and therefore may help to prevent remodelling of the airways.

Cited by 126 publications

References 51 publications

Characterization of a novel model incorporating airway epithelial damage and related fibrosis to the pathogenesis of asthma

Characterization of a novel model incorporating airway epithelial damage and related fibrosis to the pathogenesis of asthma

Increase in laminin expression in allergic airway remodelling and decrease by dexamethasone

Role of Insulin-like Growth Factor Binding Protein-3 in Allergic Airway Remodeling

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