Effects of PM2.5 components in the release of amphiregulin by human airway epithelial cells

Rumelhard, Mélina; Ramgolam, Kiran; Auger, Floriane; Dazy, Anne-Catherine; Blanchet, Sophie; Marano, Francelyne; Baeza‐Squiban, Armelle

doi:10.1016/j.toxlet.2006.11.014

Cited by 32 publications

(15 citation statements)

References 35 publications

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“…2). This strong involvement of organic components in PM2.5-induced EGFR ligand expression has already been shown for amphiregulin [13,23].…”

Section: Pm25-induced Egfr Ligands Mediate a Pro-inflammatory Responsupporting

confidence: 69%

“…Reverse transcription (RT) of 1 mg of total RNA was then performed as described by RUMELHARD et al [13], one-tenth of the RT reaction was then amplified using quantitative PCR in the presence of 1X Brilliant1 SYBR1 Green Master mix (Stratagene, La Jolla, CA, USA) and forward and reverse primers (table 2). Amphiregulin, betacellulin, HB-EGF and reduced glyceraldehyde phosphate dehydrogenase primers were purchased from Operon Biotechnologies (Cologne, Germany) and TGF-a primers from Invitrogen (Paisley, UK).…”

Section: Gene Expression Analysismentioning

confidence: 99%

“…These data, combined with the present study, performed with a bronchial cell line and nasal primary cells, underline the fact that induced release of EGFR ligands is not limited to cell lines and occurs throughout the respiratory tract: nasal and bronchial cells responding in a similar fashion. Furthermore, amphiregulin [16] and TGF-a [17] have been described as being preferentially released towards the basolateral compartment, while EGFR is localised in the basolateral membrane [13], which suggests that PM2.5-induced EGFR ligands could mediate responses of bronchial epithelial cells via an autocrine effect.…”

Section: Pm25 Induces Egfr Ligands M Rumelhard Et Almentioning

confidence: 99%

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Expression and role of EGFR ligands induced in airway cells by PM2.5 and its components

Rumelhard¹,

Ramgolam²,

Hamel³

et al. 2007

European Respiratory Journal

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The aim of the current study was to establish the epidermal growth factor receptor (EGFR) ligand expression profile in human airway epithelial cells exposed to either particulate matter (PM) with an aerodynamic diameter ,2.5 mm (PM2.5) or its components and the involvement of EGFR ligands in PM2.5-provoked airway inflammation.EGFR ligand mRNA and protein expression were studied in a human bronchial epithelial cell line and normal nasal cells exposed to noncytotoxic concentrations of PM2.5 or its components. The autocrine role of EGFR ligands in airway epithelial cell pro-inflammation was determined by adding conditioned media from PM2.5-treated cells to fresh cells and measuring the secretion of granulocyte-macrophage colony-stimulating factor (GM-CSF), a pro-inflammatory biomarker.PM2.5 increased amphiregulin, transforming growth factor-a and heparin-binding EGF-like growth factor mRNA expression and protein secretion, with a slight contribution of aqueous metallic compounds and a strong participation of organic components putatively attributed to PM polyaromatic hydrocarbon content. PM2.5-induced EGFR ligands were involved in cellular GM-CSF release.The current study revealed upregulation of several epidermal growth factor receptor ligands by airway epithelial cells exposed to particulate matter with an aerodynamic diameter ,2.5 mm and their contribution to bronchial epithelial cell granulocyte-macrophage colony-stimulating factor secretion by an autocrine action, suggesting that these ligands could elicit and sustain the particulate matter-induced airway pro-inflammatory response and contribute to bronchial remodelling.

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“…2). This strong involvement of organic components in PM2.5-induced EGFR ligand expression has already been shown for amphiregulin [13,23].…”

Section: Pm25-induced Egfr Ligands Mediate a Pro-inflammatory Responsupporting

confidence: 69%

Section: Gene Expression Analysismentioning

confidence: 99%

Section: Pm25 Induces Egfr Ligands M Rumelhard Et Almentioning

confidence: 99%

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Expression and role of EGFR ligands induced in airway cells by PM2.5 and its components

Rumelhard¹,

Ramgolam²,

Hamel³

et al. 2007

European Respiratory Journal

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“…It has been shown that ambient PM also induces epithelial cells to produce amphiregulin, granulocyte-macrophage colony-stimulating factor and MIP-3 ␣ [53][54][55][56] , that are known to induce recruitment and survival of DC. It seems likely therefore that DC will be among the first cells to sense and respond to inhaled PM, although the importance of bronchial/pulmonary epithelial cells cannot be overlooked.…”

Section: Discussionmentioning

confidence: 99%

Activation of Pulmonary Dendritic Cells and Th2-Type Inflammatory Responses on Instillation of Engineered, Environmental Diesel Emission Source or Ambient Air Pollutant Particles in vivo

et al. 2010

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The biological effects of acute particulate air pollution exposure in host innate immunity remain obscure and have relied largely on in vitro models. We hypothesized that single acute exposure to ambient or engineered particulate matter (PM) in the absence of other secondary stimuli would activate lung dendritic cells (DC) in vivo and provide information on the early immunological events of PM exposure and DC activation in a mouse model naïve to prior PM exposure. Activation of purified lung DC was studied following oropharyngeal instillation of ambient particulate matter (APM). We compared the effects of APM exposure with that of diesel-enriched PM (DEP), carbon black particles (CBP) and silver nanoparticles (AgP). We found that PM species induced variable cellular infiltration in the lungs and only APM exposure induced eosinophilic infiltration. Both APM and DEP activated pulmonary DC and promoted a Th2-type cytokine response from naïve CD4+ T cells ex vivo. Cultures of primary peribronchial lymph node cells from mice exposed to APM and DEP also displayed a Th2-type immune response ex vivo. We conclude that exposure of the lower airway to various PM species induces differential immunological responses and immunomodulation of DC subsets. Environmental APM and DEP activated DC in vivo and provoked a Th2 response ex vivo. By contrast, CBP and AgP induced altered lung tissue barrier integrity but failed to stimulate CD4+ T cells as effectively. Our work suggests that respirable pollutants activate the innate immune response with enhanced DC activation, pulmonary inflammation and Th2-immune responsiveness.

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“…There is a growing interest in the origin and characteristics of atmospheric particles and the potentially harmful effects they have on living things (Rumelhard et al 2007). The relationship between ambient concentrations of fine particulate matter and detrimental health effects is still a highly controversial issue.…”

Section: Introductionmentioning

confidence: 99%

Toxic Metals (As, Cd, Ni and Pb) and PM2.5 in Air Concentration of a Model Ceramic Cluster

Vicente

Pallarés

Soriano

et al. 2011

Water Air Soil Pollut

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The relationship between ambient concentrations of fine particulate matter and detrimental health effects remains a highly controversial issue. Increased incidence of mortality and morbidity due to cardiopulmonary complications has been associated with elevated levels of urban air particles with an aerodynamic of <2.5 μm (PM2.5). The main aim of this paper was to present the assessment of the temporal and spatial variations of the PM2.5 fraction and its contents in arsenic, cadmium, nickel and lead in order to identify possible emission sources of these pollutants. Daily ambient aerosol samples (PM2.5) were taken in the province of Castellón from 2008 to 2009. Particle concentration levels were determined by gravimetry, and the As, Cd, Ni and Pb levels in the samples were determined by inductively coupled plasma mass spectroscopy. The season variation of these pollutants differs according to the emission source and the factors involved in dispersion. In the weekly trend, there were no significant differences in levels among sampling sites in relation to the day activity (working vs. non-working) due to chemical pollutants that are found in fine particulate fractions residing in the atmosphere longer than coarse particles, resulting in a more homogeneous concentration of pollutants over time. In order to identify similar behaviour between chemical pollutants and PM2.5, an assessment of the correlation between them was carried out. This behaviour study shows whether the source of contaminants is the same. A statistical analysis of the levels of PM2.5 and the presence of As, Cd, Ni and Pb in the different sampling sites was performed in order to evaluate the influence of the sampling point on the concentrations of these pollutants.

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Effects of PM2.5 components in the release of amphiregulin by human airway epithelial cells

Cited by 32 publications

References 35 publications

Expression and role of EGFR ligands induced in airway cells by PM2.5 and its components

Expression and role of EGFR ligands induced in airway cells by PM2.5 and its components

Activation of Pulmonary Dendritic Cells and Th2-Type Inflammatory Responses on Instillation of Engineered, Environmental Diesel Emission Source or Ambient Air Pollutant Particles in vivo

Toxic Metals (As, Cd, Ni and Pb) and PM2.5 in Air Concentration of a Model Ceramic Cluster

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