br Conflict of interest statement br

Conflict of interest statement
Author contributions The following are the supplementary data related to this purchase HBTU article
Acknowledgements We thank the NIAID Tetramer Facility (Emory University, Atlanta, GA) for supplying CD1d tetramer and Dr. T. Camou (National Reference Laboratory, Ministry of Health, Montevideo, Uruguay) for the gift of the S. pneumoniae serotype 1 clinical isolate E1586. We also thank Hélène Bauderlique for her help for cell sorting (BICel Cytométrie Plateform, Institut Pasteur de Lille, France). A special thank to Gwénola Kervoaze and Eva Vilain for their technical support, and Jean-Claude Sirard, François Trottein, Isabelle Wolowczuk and Sandra Weller for their critical reviewing of the paper. This work was supported by the Institut National de la Santé et de la Recherche Médicale (Inserm), the Centre National de la Recherche Scientifique (CNRS) and the Conseil Régional du Nord-Pas de Calais [StreptoCOPD project; grant number # 13005300]. Funders had no role in study design, data collection, data analysis, interpretation, writing of the report.
Introduction At the dawn of the 21st century air pollution remains a growing public health threat (Lim et al., 2013), regardless of the fact that air quality should be regarded as an integral part of human rights (Samet and Gruskin, 2014). Among air pollutants, fine particulate matters (PMs) of less than 2·5μm in diameter (PM2.5) were recently ranked as one of the leading causes of death and disability worldwide (Lim et al., 2013). Recent studies indicate the persistence of adverse health effects and associate long-term exposure to PM2.5 with natural-cause mortality even within concentrations below those recommended by the WHO and European institutions (Beelen et al., 2014). According to epidemiological studies, long-term exposure to high concentrations of PM increases the risk of cardiovascular (Pope et al., 2009; Shah et al., 2013) and respiratory disease (Zemp et al., 1999), diabetes (Li et al., 2014) and lung cancer (Raaschou-Nielsen et al., 2013), whereas short-term exposure can exacerbate and/or onset various forms of respiratory disease, such as asthma (Guarnieri and Balmes, 2014; Gordon et al., 2014; Smith et al., 2000). A recent review discussed clinical implications, policy issues, and research gaps relevant to air pollution and asthma (Guarnieri and Balmes, 2014). One of the most challenging tasks for air pollution research has been how to address the fact that people are almost always exposed to a mixture of pollutants (Kelly and Fussell, 2012). Concerning exposure to PM2.5 the authors note that the most responsible components of the particulate mix are not known and they add that unraveling which components of the traffic pollution mixture are responsible for asthma exacerbations and onset is a substantial challenge (Guarnieri and Balmes, 2014). Obviously, this discussion may also apply to other adverse health effects such as cardiovascular disease and lung cancer. Among particulate constituents, carbon, found in alveolar macrophages (AM), has been linked in a dose dependent manner to the decline in lung function (Kulkarni et al., 2006). In addition, a recent study suggested a possible mechanism underlying the observation that traffic-derived air pollution adversely affects children with asthma, because they may be less able to clear inhaled PM effectively (Brugha et al., 2014). In both studies, macrophage carbon content was assessed with image analysis of black material present inside AM, visualized with optical microscopy alone. Yet, based on empirical evidence, we postulate that lamellar bodies and carbon content cannot be distinguished by optical microscopy, and even low magnification transmission electron microscopy (TEM) because their sizes and aspects are quite similar. Hence, in order to unravel which components of carbonaceous PM are responsible for adverse effects, it is first important to thoroughly and specifically characterize the components present in the “black material inside AM”.