Induction of IL-6 and inhibition of IL-8 secretion in the human airway cell line Calu-3 by urban particulate matter collected with a modified method of PM sampling

Alfaro-Moreno, Ernesto; Torres, Víctor Eduardo; Miranda, J.; Martínez, Leticia; García-Cuéllar, Claudia M.; Nawrot, Tim S.; Vanaudenaerde, Bart M.; Hoet, Peter; Ramírez-López, Pavel; Rosas, Irma; Nemery, Benoît; Osornio-Vargas, Álvaro

doi:10.1016/j.envres.2009.02.010

Cited by 82 publications

(50 citation statements)

References 30 publications

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“…Indeed, exposure to concentrated PM results in the release of pro-inflammatory cytokines such as IL-6 or TNFα from alveolar 32 or peritoneal 33 macrophages. Similarly, human airway cells 34 or bronchial epithelial cells 35 release TNFα, IL-6 or IL-8 upon incubation of ambient air particles. Our observation showing that circulating levels of TNFα, IL-8, and IL-6 are increased upon PM 2.5 inhalation is consistent with the possibility that the release of cytokines in the lung could trigger and sustain a state of mild systemic inflammation.…”

Section: Discussionmentioning

confidence: 99%

Exposure to Fine Particulate Air Pollution Is Associated With Endothelial Injury and Systemic Inflammation

Pope

Bhatnagar

McCracken

et al. 2016

Circulation Research

529

278

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Rationale Epidemiologic evidence indicates that exposures to fine particulate matter air pollution (PM2.5) contribute to global burden of disease, primarily as a result of increased risk of cardiovascular morbidity and mortality. However, mechanisms by which PM2.5 exposure induces cardiovascular injury remain unclear. PM2.5-induced endothelial dysfunction and systemic inflammation have been implicated, but direct evidence is lacking. Objective To examine whether acute exposure to PM2.5 is associated with endothelial injury and systemic inflammation. Methods and Results Blood was collected from healthy, non-smoking, young adults over three study periods that included episodes of elevated PM2.5 levels. Microparticles and immune cells in blood were measured by flow cytometry, and plasma cytokine/growth factors were measured using multiplexing laser beads. PM2.5 exposure was associated with elevated levels of endothelial microparticles (annexin V+/CD41−/CD31+) including subtypes expressing arterial-, venous-, and lung-specific markers, but not microparticles expressing CD62+. These changes were accompanied by suppressed circulating levels of pro-angiogenic growth factors (EGF, sCD40L, PDGF, RANTES, GROα, and VEGF), and an increase in the levels of anti-angiogenic (TNFα, IP-10) and proinflammatory cytokines (MCP-1, MIP-1α/β, IL-6, and IL-1β), and markers of endothelial adhesion (sICAM-1 and sVCAM-1). PM2.5 exposure also was associated with an inflammatory response characterized by elevated levels of circulating CD14+, CD16+, CD4+, and CD8+, but not CD19+ cells. Conclusions Episodic PM2.5 exposures are associated with increased endothelial cell apoptosis, an anti-angiogenic plasma profile, and elevated levels of circulating monocytes, and T, but not B, lymphocytes. These changes could contribute to the pathogenic sequelae of atherogenesis and acute coronary events.

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Section: Discussionmentioning

confidence: 99%

Exposure to Fine Particulate Air Pollution Is Associated With Endothelial Injury and Systemic Inflammation

Pope

Bhatnagar

McCracken

et al. 2016

Circulation Research

529

278

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“…In parallel with the ambient air monitoring, and according to Alfaro-Moreno et al [25] we collected PM 2.5 , at the same schedule of animal exposure, in cellulose- nitrate membranes with home-made modifications using HiVol samplers, in order to obtain large quantities of PM 2.5 to determine endotoxin content and reactive oxidant activity using the DTT assay in the PM 2.5 samples.…”

Section: Methodsmentioning

confidence: 99%

Early kidney damage induced by subchronic exposure to PM2.5 in rats

et al. 2016

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BackgroundParticulate matter exposure is associated with respiratory and cardiovascular system dysfunction. Recently, we demonstrated that fine particles, also named PM2.5, modify the expression of some components of the angiotensin and bradykinin systems, which are involved in lung, cardiac and renal regulation. The endocrine kidney function is associated with the regulation of angiotensin and bradykinin, and it can suffer damage even as a consequence of minor alterations of these systems. We hypothesized that exposure to PM2.5 can contribute to early kidney damage as a consequence of an angiotensin/bradykinin system imbalance, oxidative stress and/or inflammation.ResultsAfter acute and subchronic exposure to PM2.5, lung damage was confirmed by increased bronchoalveolar lavage fluid (BALF) differential cell counts and a decrease of surfactant protein-A levels. We observed a statistically significant increment in median blood pressure, urine volume and water consumption after PM2.5 exposure. Moreover, increases in the levels of early kidney damage markers were observed after subchronic PM2.5 exposure: the most sensitive markers, β-2-microglobulin and cystatin-C, increased during the first, second, sixth and eighth weeks of exposure. In addition, a reduction in the levels of specific cytokines (IL-1β, IL-6, TNF-α, IL-4, IL-10, INF-γ, IL-17a, MIP-2 and RANTES), and up-regulated angiotensin and bradykinin system markers and indicators of a depleted antioxidant response, were also observed. All of these effects are in concurrence with the presence of renal histological lesions and an early pro-fibrotic state.ConclusionSubchronic exposure to PM2.5 induced an early kidney damage response that involved the angiotensin/bradykinin systems as well as antioxidant and immune imbalance. Our study demonstrates that PM2.5 can induce a systemic imbalance that not only affects the cardiovascular system, but also affects the kidney, which may also overall contribute to PM-related diseases.Electronic supplementary materialThe online version of this article (doi:10.1186/s12989-016-0179-8) contains supplementary material, which is available to authorized users.

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“…Indeed, both carbon nanotubes and urban particulate matter are responsible for the activation of proinflammatory pathways in macrophages, with robust acute inflammatory responses leading to a rapid onset of chronic lung fibrosis, extensive granulomas, and other pathologies. [3][4][5][6] Moreover, these systems, as well as metal and silica nanoparticles, induce oxidative stress associated with an increase in reactive oxygen species production and the expression of antioxidant enzymes. 7,8 It has been further shown that the toxicological profile and biological response to the different nanoparticles are closely correlated with their physicochemical properties because, for instance, amorphous silica nanoparticles have a different toxicity profile compared with the crystalline ones.…”

Section: Introductionmentioning

confidence: 99%

“…[50][51][52] To assess the in vitro toxicity of the nanoparticles, we chose the Calu-3 cell line previously used to assess the toxicological profiles of environmental matter and colloidal systems. 6 The Calu-3 cell line derives from a human adenocarcinoma, and constitutes a well established in vitro model of lung epithelium. 21 Calu-3 cells secrete mucus and have apically located cilia mimicking the physiological conditions of the upper airways.…”

mentioning

confidence: 99%

Influence of surface charge on the potential toxicity of PLGA nanoparticles towards Calu-3 cells

Mura¹,

Hillaireau²,

Nicolas³

et al. 2011

IJN

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Background Because of the described hazards related to inhalation of manufactured nanoparticles, we investigated the lung toxicity of biodegradable poly (lactide-co-glycolide) (PLGA) nanoparticles displaying various surface properties on human bronchial Calu-3 cells. Methods Positively and negatively charged as well as neutral nanoparticles were tailored by coating their surface with chitosan, Poloxamer, or poly (vinyl alcohol), respectively. Nanoparticles were characterized in terms of size, zeta potential, and surface chemical composition, confirming modifications provided by hydrophilic polymers. Results Although nanoparticle internalization by lung cells was clearly demonstrated, the cytotoxicity of the nanoparticles was very limited, with an absence of inflammatory response, regardless of the surface properties of the PLGA nanoparticles. Conclusion These in vitro results highlight the safety of biodegradable PLGA nanoparticles in the bronchial epithelium and provide initial data on their potential effects and the risks associated with their use as nanomedicines.

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Induction of IL-6 and inhibition of IL-8 secretion in the human airway cell line Calu-3 by urban particulate matter collected with a modified method of PM sampling

Cited by 82 publications

References 30 publications

Exposure to Fine Particulate Air Pollution Is Associated With Endothelial Injury and Systemic Inflammation

Exposure to Fine Particulate Air Pollution Is Associated With Endothelial Injury and Systemic Inflammation

Early kidney damage induced by subchronic exposure to PM2.5 in rats

Influence of surface charge on the potential toxicity of PLGA nanoparticles towards Calu-3 cells

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