Neutrophils infiltrating bronchial epithelium in chronic obstructive pulmonary disease

Pesci, Alberto; Majori, Maria; Cuomo, Angelo; Borciani, N; Bertacco, Stefano; Cacciani, Giancarlo; Gabrielli, M

doi:10.1016/s0954-6111(98)90389-4

Cited by 73 publications

(51 citation statements)

References 31 publications

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“…RBM thickness and composition in asthma and COPD status. 1,5,7,[9][10][11][12][13]15,17,22, Taken together, we conclude that an increased RBM thickness indicates the presence of asthma or COPD, irrespective of age and that it is not possible to differentiate mild-to-moderate asthma from COPD purely based on RBM thickness. In addition, a normal RBM thickness does not exclude obstructive airway disease.…”

Section: Discussionmentioning

confidence: 70%

“…Some studies fi nd a normal RBM, [6][7][8] while others report it to be thickened, [9][10][11][12][13] but generally to a smaller extent than in asthma. 9,10,12,14,15 The differences in observations may be due to the fact that some studies have included only a few COPD patients 7 or COPD patients with only mild 10 or more severe 9 airway obstruction.…”

Section: Introductionmentioning

confidence: 99%

“…9,10,12,14,15 The differences in observations may be due to the fact that some studies have included only a few COPD patients 7 or COPD patients with only mild 10 or more severe 9 airway obstruction. In addition, some studies included healthy controls who were either never smokers 11 or smokers not being matched for pack-years smoking. 8 Airway infl ammation is of a chronic nature in both asthma and COPD, likely resulting in a long-lasting increase of fi brogenic growth factors like transforming growth factor-β in both asthma and COPD, 10,16 vascular endothelial growth factor in asthma, 17 and epidermal growth factors in COPD.…”

Section: Introductionmentioning

confidence: 99%

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Reticular basement membrane in asthma and COPD: Similar thickness, yet different composition

Liesker

Hacken

Zeinstra-Smith³

et al. 2009

COPD

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Background: Reticular basement membrane (RBM) thickening has been variably associated with asthma and chronic obstructive pulmonary disease (COPD). Even if RBM thickness is similar in both diseases, its composition might still differ. Objective: To assess whether RBM thickness and composition differ between asthma and COPD. Methods: We investigated 24 allergic asthmatics (forced expiratory volume in one second [FEV 1 ] 92% predicted), and 17 nonallergic COPD patients (FEV 1 60% predicted), and for each group a control group of similar age and smoking habits (12 and 10 persons, respectively). Snapfrozen sections of bronchial biopsies were stained with hematoxylin/eosin and for collagen I, III, IV, V, laminin and tenascin. RBM thickening was assessed by digital image analysis. Relative staining intensity of each matrix component was determined. Results: Mean (SD) RBM thickness was not signifi cantly different between asthma and COPD 5.5 (1.3) vs 6.0 (1.8) μm, but signifi cantly larger than in their healthy counterparts, ie, 4.7 (0.9) and 4.8 (1.2) μm, respectively. Collagen I and laminin stained signifi cantly stronger in asthma than in COPD. Tenascin stained stronger in asthma than in healthy controls of similar age, and stronger in COPD controls than in asthma controls (p Ͻ 0.05). Conclusion: RBM thickening occurs both in asthma and COPD. We provide supportive evidence that its composition differs in asthma and COPD.

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Section: Discussionmentioning

confidence: 70%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Reticular basement membrane in asthma and COPD: Similar thickness, yet different composition

Liesker

Hacken

Zeinstra-Smith³

et al. 2009

COPD

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“…The discordance of these results with those showing an increase in numbers of neutrophils and markers of neutrophil activation in bronchoalveolar lavage [10,11,13,14,25], induced sputum [26±28] and airway epithelium [29] remains to be explained.…”

Section: Discussionmentioning

confidence: 82%

Subepithelial immunopathology of the large airways in smokers with and without chronic obstructive pulmonary disease

2000

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Previous work has shown an increase in CD8+ T-cells, neutrophils and eosinophils in small airway subepithelium in smokers. The authors have now investigated whether similar changes occur in the large airways.Immunohistochemistry on frozen sections of bronchial biopsies were obtained at bronchoscopy in 11 nonsmokers, eight asymptomatic smokers and 11 smokers with chronic bronchitis and chronic obstructive pulmonary disease (COPD).There was an increase in the number of CD8+ cells infiltrating the bronchial subepithelium in the COPD group compared to the asymptomatic smokers (305 (109± 400) versus 92 (41±550) cells . mm -2 , p=0.030). There was a negative correlation between the number of CD8+ cells and the forced expiratory volume in one second (FEV1) %predicted (p=0.005, r=-0.62), and a positive correlation between the number of CD8+ cells and the number of pack years smoked (p=0.017, r=0.42). There was a negative correlation between the activated/total eosinophils ratio and the FEV1 % pred (p=0.017, r=-0.51). There was a negative correlation between pack years smoked and the number of neutrophils (p=0.022, r=-0.36).Smokers who develop chronic obstructive pulmonary disease have increased numbers of CD8+ T-cells in large airways when compared to asymptomatic smokers. Airway obstruction was associated with an increase in the proportion of eosinophils that were activated. Eur Respir J 2000; 15: 512±516.

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“…COPD is characterised by irreversible airflow obstruction and progressive lung inflammation that correlates with disease severity [2]. Whilst asthma is more associated with eosinophilic inflammation, in COPD, neutrophils and macrophages predominate [3].…”

mentioning

confidence: 99%

A mouse GM-CSF receptor antibody attenuates neutrophilia in mice exposed to cigarette smoke

et al. 2011

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We investigated the role of granulocyte-macrophage colony-stimulating factor (GM-CSF) in a subchronic exposure model of cigarette smoke (CS)-induced inflammation using antibodies directed against GM-CSF or the GM-CSF receptor (GM-CSFR) a-chain.CS-induced mononuclear and neutrophilic inflammation following 4 days of CS exposure in BALB/c mice was assessed in bronchoalveolar lavage (BAL) fluid. An increase in mature dendritic cells (DCs) (CD11c+ and major histocompatibility complex II+) and Gr-1-high neutrophils was also observed by flow cytometric analysis of whole-lung tissue.Daily i.p. injection of 400 mg GM-CSF or GM-CSFR antibody prior to daily smoke exposure attenuated the accumulation of neutrophils within the BAL by 60%. A reduction in mature DCs was also observed. Anti-GM-CSFR antibody administration did not have an effect on the percentage of lung T-cells; however, a significant decrease in activated CD69+ CD8+ T-cells was observed. Anti-GM-CSFR antibody administration decreased the mRNA and protein expression of interleukin-12 p40 and matrix metalloproteinase 12.Taken together, intervention with this receptor antibody implicates the GM-CSF pathway as an important mediator of smoke-induced inflammation.

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Neutrophils infiltrating bronchial epithelium in chronic obstructive pulmonary disease

Cited by 73 publications

References 31 publications

Reticular basement membrane in asthma and COPD: Similar thickness, yet different composition

Reticular basement membrane in asthma and COPD: Similar thickness, yet different composition

Subepithelial immunopathology of the large airways in smokers with and without chronic obstructive pulmonary disease

A mouse GM-CSF receptor antibody attenuates neutrophilia in mice exposed to cigarette smoke

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