Smoke Extract Stimulates Lung Epithelial Cells to Release Neutrophil and Monocyte Chemotactic Activity

Masubuchi, Takeshi; Koyama, Sekiya; Sato, Etsuro; Takamizawa, Akemi; Kubo, Keishi; Sekiguchi, Morie; Nagai, Sonoko; Izumi, Tohru

doi:10.1016/s0002-9440(10)65704-5

Cited by 130 publications

(110 citation statements)

References 35 publications

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“…This result is consistent with other reported data. Indeed, in vitro studies showed that chemokines released by cultured cells were significantly increased in response to smoke (30,31 ) and smokeless tobacco extracts (32 ). Deo et al (20 ) found a positive correlation between smoking and plasma MCP-1 concentrations in adults in a large probability-based population.…”

Section: Discussionmentioning

confidence: 99%

Biological Determinants of and Reference Values for Plasma Interleukin-8, Monocyte Chemoattractant Protein-1, Epidermal Growth Factor, and Vascular Endothelial Growth Factor: Results from the STANISLAS Cohort

et al. 2006

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Background: Interleukin-8 (IL-8), monocyte chemoattractant protein-1 (MCP-1), epidermal growth factor (EGF), and vascular endothelial growth factor (VEGF) are known to be involved in various diseases related to inflammation, vascular remodeling, or growth deregulation. In addition, increases in plasma concentrations of these cytokines appear to provide useful diagnostic and prognostic information. We therefore investigated which factors most strongly influence the biological variations of plasma IL-8, MCP-1, EGF, and VEGF concentrations. Methods: We used the Evidence ® biochip array analyzer to quantify plasma IL-8, MCP-1, EGF, and VEGF concentrations in a subsample of 304 children (age range, 4 -17 years) and 540 adults (age range, 18 -55 years) from the STANISLAS family study. We also calculated reference intervals for the 4 cytokines. Results: We found the following associations with plasma marker concentrations: Age, neutrophil count, and glucose concentration were positively associated with IL-8 concentrations in children and adults, as were smoking and platelet count in adults. MCP-1 concentrations were associated with age and smoking in both children and adults, monocyte count in children, and sex and hematocrit in adults. EGF concentrations were

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Section: Discussionmentioning

confidence: 99%

Biological Determinants of and Reference Values for Plasma Interleukin-8, Monocyte Chemoattractant Protein-1, Epidermal Growth Factor, and Vascular Endothelial Growth Factor: Results from the STANISLAS Cohort

et al. 2006

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“…Moreover, the concomitant release of neutrophil and monocyte chemotactic activity i.e. IL-8, granulocyte-colony stimulating factor, monocyte chemotactic peptide-1, and granulocyte-macrophage colony-stimulating factor, from airway epithelial cells in response to IL-1b, TNF-a, LPS, SE and BK, was reported [24][25][26][27][28]. Thus, airway epithelial cells may regulate the permeability of lung blood vessels in the inflammatory lung diseases in combination with inflammatory cell recruitment.…”

Section: Discussionmentioning

confidence: 99%

“…SE was prepared by the methods of JANOFF and CARP [23]. The concentrations of LPS, IFN-c, SE, NE and BK were high enough to induce the release of neutrophil and monocyte chemotactic factors from A549 cells and BEAS-2B cells [24][25][26][27][28]. In these stimuli, the concentration of LPS was v10 ng?mL -1 at the maximum stimulant concentration.…”

Section: Airway and Alveolar Epithelial Cell Preparationmentioning

confidence: 99%

Vascular endothelial growth factor mRNA and protein expression in airway epithelial cell linesin vitro

Koyama¹,

Sato²,

Tsukadaira³

et al. 2002

Eur Respir J

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Vascular endothelial growth factor (VEGF) plays multifunctional roles in vascular permeability, repair and remodelling processes, in addition to the maintenance of vascular structure and function. In the present study, the potential of airway epithelial cell lines, BEAS-2B cells and A549 cells, to release and express VEGF in unstimulated and stimulated conditions was evaluated.The secretion and expression of VEGF were evaluated by enzyme-linked immunosorbant assay and by reverse transcriptase-polymerase chain reaction. The isoforms of released VEGF were determined by high-performance liquid chromatography.BEAS-2B cells and A549 cells released VEGF constitutively. Interleukin (IL)-1β and tumour necrosis factor (TNF)-α augmented the release of VEGF in a time- and dose-dependent manner. The released VEGF was 165 amino acid residues in either condition.Pseudomonas aeruginosalipopolysaccharide (LPS), interferon (IFN)-γ, smoke extract (SE), neutrophil elastase (NE), and bradykinin stimulated the release of VEGF. Keracinocyte growth factor (KGF), which reduces vascular permeability, also stimulated both cells to release VEGF. VEGF messenger ribonucleic acid (mRNA) was expressed both time- and dose-dependently at 2 h, and declined after 2 h in response to IL-1β and TNF-α. The expression of VEGF mRNA in airway epithelial cells was also augmented by LPS, IFN-γ, SE, NE, and KGF stimulation.These data suggest that airway epithelial cells may regulate the maintenance of vascular structure and function, as well as vascular permeability, repair and remodelling processes, in a variety of lung conditions by expressing vascular endothelial growth factor.

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“…The bronchiolar epithelium is altered in smokers, particularly in patients with COPD. Cigarette smoke induces the release of interleukin (IL)-1, IL-8, and granulocyte colony-stimulating factor from bronchial epithelial cells through oxidative pathways, accounting for potential neutrophil and monocytic chemotactic activities released from the epithelium (5,6). A higher expression of monocyte chemotactic protein-1, transforming growth factor (TGF)-␤1, and IL-8 mRNA and protein has been observed in bronchiolar epithelium of smokers with COPD compared with smokers without COPD (7)(8)(9).…”

Section: Epithelial Changesmentioning

confidence: 99%

The Role of Airway Smooth Muscle in the Pathogenesis of Airway Wall Remodeling in Chronic Obstructive Pulmonary Disease

Chung¹

2005

Proceedings of the American Thoracic Society

105

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Airway wall remodeling processes are present in the small airways of patients with chronic obstructive pulmonary disease, consisting of tissue repair and epithelial metaplasia that contribute to airway wall thickening and airflow obstruction. With increasing disease severity, there is also increased mucous metaplasia and submucosal gland hypertrophy, peribronchial fibrosis, and an increase in airway smooth muscle mass. Apart from its contractile properties, airway smooth muscle produces inflammatory cytokines, proteases, and growth factors, which may contribute to the remodeling process and induce phenotypic changes of the muscle. Airflow limitation responds minimally to ␤-agonists and corticosteroid therapy, unlike asthma, perhaps because of alterations in ␤-receptor or glucocorticoid receptor numbers, alterations in receptor signaling, or the constrictive limitation imposed by peribronchial fibrosis. Better response is observed with the combination of inhaled long-acting ␤-agonists and corticosteroids. This could result from effects at the level of airway smooth muscle. Airway wall remodeling may involve the release of growth factors from inflammatory or resident cells. The influence of smoking cessation or of current therapies on airway wall remodeling is unknown. Specific therapies for airway wall remodeling may be necessary, together with noninvasive methods of imaging small airway wall remodeling to assess responses.

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Smoke Extract Stimulates Lung Epithelial Cells to Release Neutrophil and Monocyte Chemotactic Activity

Cited by 130 publications

References 35 publications

Biological Determinants of and Reference Values for Plasma Interleukin-8, Monocyte Chemoattractant Protein-1, Epidermal Growth Factor, and Vascular Endothelial Growth Factor: Results from the STANISLAS Cohort

Biological Determinants of and Reference Values for Plasma Interleukin-8, Monocyte Chemoattractant Protein-1, Epidermal Growth Factor, and Vascular Endothelial Growth Factor: Results from the STANISLAS Cohort

Vascular endothelial growth factor mRNA and protein expression in airway epithelial cell linesin vitro

The Role of Airway Smooth Muscle in the Pathogenesis of Airway Wall Remodeling in Chronic Obstructive Pulmonary Disease

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