Publications Scientifiques

[ Article ] Proinflammatory effects and oxidative stress within human bronchial epithelial cells exposed to atmospheric particulate matter (PM2.5 and PM>2.5) collected from Cotonou, Benin

Date de soumission: 23-02-2018
Année de Publication: 2014
Entité/Laboratoire Laboratoire de Biochimie et de Biologie Moléculaire (LBBM)
Document type : Article
Discipline(s) : Biochimie, biophysique & Biologie Moléculaire
Titre Proinflammatory effects and oxidative stress within human bronchial epithelial cells exposed to atmospheric particulate matter (PM2.5 and PM>2.5) collected from Cotonou, Benin
Auteurs Cachon Boris Fresnel [1], Stéphane Firmin b,d [2], Verdin Anthony b [3], Ayi-Fanou Lucie [4], Billet Sylvain a,b [5], Cazier Fabrice [6], Martin Perrine J, a,b [0],
Journal: Environmental Pollution
Catégorie Journal: Internationale
Impact factor: 0
Volume Journal: 185
DOI: 10.1016/j.envpol.2013.10.026
Resume After particulate matter (PM) collection in Cotonou (Benin), a complete physicochemical characterization of PM2.5 and PM>2.5 was led. Then, their adverse health effects were evaluated by using in vitro culture of human lung cells. BEAS-2B (bronchial epithelial cells) were intoxicated during short-term exposure at increasing PM concentrations (1.5-96 μg/cm(2)) to determine global cytotoxicity. Hence, cells were exposed to 3 and 12 μg/cm(2) to investigate the potential biological imbalance generated by PM toxicity. Our findings showed the ability of both PM to induce oxidative stress and to cause inflammatory cytokines/chemokines gene expression and secretion. Furthermore, PM were able to induce gene expression of enzymes involved in the xenobiotic metabolism pathway. Strong correlations between gene expression of metabolizing enzymes, proinflammatory responses and cell cycle alteration were found, as well as between proinflammatory responses and cell viability. Stress oxidant parameters were highly correlated with expression and protein secretion of inflammatory mediators.
Mots clés Benin; Cytotoxicity; Inflammatory response; Oxidative stress; Particulate matter
Pages 340 - 351
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