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<title lang=en>POSTER 40 Is oxidative stress responsible for plasma membrane integrity alteration in macrophages from patients with cystic fibrosis?</title>
<creator>Le Trionnaire, S.</creator>
<creator>Lévêque, M.</creator>
<creator>Belleguic, C.</creator>
<creator>Deneuville, E.</creator>
<creator>Desrues, B.</creator>
<creator>Brinchault, G.</creator>
<creator>Dabadie, A.</creator>
<creator>Roussey, M.</creator>
<creator>Jouneau, S.</creator>
<creator>Gangneux, J. -P.</creator>
<creator>Dimanche-Boitrel, M. -T.</creator>
<creator>Martin-Chouly, C</creator>
<contributor>Centre de Ressource et de Compétences de la Mucoviscidose ; Université de Rennes 1 (UR1) - CHU Pontchaillou [Rennes]</contributor>
<contributor>Service de pneumologie ; Université de Rennes 1 (UR1) - CHU Pontchaillou [Rennes]</contributor>
<contributor>Service de Pédiatrie ; Hôpital Pontchaillou - CHU Pontchaillou [Rennes]</contributor>
<contributor>Franche-Comté Électronique Mécanique, Thermique et Optique - Sciences et Technologies (FEMTO-ST) ; Université de Technologie de Belfort-Montbeliard (UTBM) - Ecole Nationale Supérieure de Mécanique et des Microtechniques (ENSMM) - Centre National de la Recherche Scientifique (CNRS) - Université de Franche-Comté (UFC)</contributor>
<contributor>Institut de recherche, santé, environnement et travail [Rennes] (Irset) ; Université d'Angers (UA) - Université des Antilles et de la Guyane (UAG) - Université de Rennes 1 (UR1) - École des Hautes Études en Santé Publique [EHESP] (EHESP) - Institut National de la Santé et de la Recherche Médicale (INSERM) - Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique )</contributor>
<description>International audience</description>
<source>the 38th European Cystic Fibrosis Conference</source>
<coverage>Vienne, Austria</coverage>
<identifier>hal-01162769</identifier>
<identifier>https://hal-univ-rennes1.archives-ouvertes.fr/hal-01162769</identifier>
<source>https://hal-univ-rennes1.archives-ouvertes.fr/hal-01162769</source>
<source>the 38th European Cystic Fibrosis Conference, Apr 2015, Vienne, Austria. 14, Supplement 1, pp.S67, 2015, 〈10.1016/S1569-1993(15)30217-4〉</source>
<identifier>DOI : 10.1016/S1569-1993(15)30217-4</identifier>
<relation>info:eu-repo/semantics/altIdentifier/doi/10.1016/S1569-1993(15)30217-4</relation>
<language>en</language>
<subject>[SDV] Life Sciences [q-bio]</subject>
<type>info:eu-repo/semantics/conferenceObject</type>
<type>Poster communications</type>
<description lang=en>Objective Oxidative stress, excess production of reactive oxygen species (ROS) and intense colonization of the respiratory tract by microorganisms are described in CF patients, leading to an influx in macrophages. This results in activation of NADPH oxidase that yields ROS, initiating the oxidative burst responsible for pathogen destruction. We showed that phagocytosis was altered in CF macrophages, yet oxidative status in this cell was not defined. The objective of this study is to draw a link between oxidative stress and plasma membrane integrity in CF macrophages, since lipid peroxidation is known to alter cell membrane. Methods Peripheral blood monocytes-derived macrophages were obtained from CF patients and healthy subjects. Plasma membrane fluidity was assessed with di4-ANEPPDHQ and oxidative status was measured with ROS indicating probes. Results In CF macrophages, membrane fluidity was increased whereas lipid peroxidation was diminished. Surprisingly, general oxidative status remained similar to the one observed in non-CF macrophages. Also, CF macrophages did not abolish chemically induced-oxidative stress. In non-CF macrophages, treatment with cholesterol slightly increased membrane fluidity whereas LPS treatment had no effect. Conclusion CF macrophages displayed an increased membrane fluidity associated with a decreased lipid peroxidation. This raises the hypothesis that membrane alteration in CF macrophages may be due to other mechanism than oxidative stress. Nevertheless, since the killing capacity of CF macrophage is defective, a deregulation of O•−2 production is very likely, suggesting alteration of NADPH oxidase or mitochondrial dysfunction</description>
<date>2015-04-22</date>
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