Search

Cette table ronde a été organisée par Jean-Yves Authier autour de deux numéros d’Espaces et sociétés : « L’espace des classes moyennes » (no 148-149, 2012) et « Où est passé le peuple ? » (no 156-157, 2014) – et plus secondairement autour de deux autres numéros plus anciens : « Usages populaires de l’espace » (no 144-145, 2011) et « La gentrification urbaine » (no 132-133, 2008). Son enjeu était double : discuter du contenu de ces numéros et de leur réception ; débattre plus largement de l’approche matérielle et spatiale des classes sociales, de ses intérêts et de ses limites.Elle a réuni, à Paris, le 22 mai 2019, autour de Jean-Yves Authier, quatre intervenant·es :Deux contributrices aux numéros cités : Anaïs Collet, maîtresse de conférences en sociologie à la faculté des sciences sociales de l’université de Strasbourg et membre du laboratoire SAGE, auteure dans « L’espace des classes moyennes » de l’article intitulé « Le loft : habitat atypique et innovation sociale pour deux générations de “nouvelles classes moyennes” » ; et Cécile Vignal, maîtresse de conférences en sociologie à l’université de Lille, rattachée au laboratoire Clersé, coauteure dans le numéro « Où est passé le peuple » de l’article intitulé « Comment étudier les classes populaires aujourd’hui ? Une démarche d’ethnographie comparée ».Deux personnalités extérieures à ces deux numéros et à Espaces et sociétés : Marie-Christine Jaillet, géographe spécialisée dans les études urbaines, directrice de recherche au CNRS, rattachée au laboratoire LISST, qui a mené de nombreux travaux sur le lien entre périurbanisation et couches moyennes ; et Olivier Schwartz, sociologue, professeur émérite à l’université Paris Descartes, qui a consacré ses travaux de recherche au monde ouvrier et aux classes dites populaires.La table ronde a été structurée en trois temps : un premier consacré à la production des deux numéros ; un deuxième centré sur leur contenu et leur réception ; et un troisième, enfin, sur les intérêts et limites d’une approche des classes sociales par l’espace.

The ubiquitous and growing presence of microplastics (MPs) in all compartments of the environment raises concerns about their possible harmful effects on human health. Human exposure to MPs occurs largely through ingestion. Polyethylene (PE) is widely employed for reusable bags and food packaging and found to be present in drinking water and food. It is also one of the major polymers detected in human stool. The aim of this study was to characterize the effects of intestinal exposure to PE MPs on gut homeostasis. Mice were orally exposed for 6 weeks to PE microbeads of 2 different sizes, 36 and 116 μm, that correspond to those found in human stool. They were administrated either individually or as a mixture at a dose of 100 μg/g of food. Both PE microbead sizes were detected in mouse stool. Different parameters related to major intestinal functions were compared between control mice, mice exposed to each type of microbead, or co-exposed to the 2 types of microbeads. Intestinal disturbances were observed after individual exposure to each size of PE microbead, and the most marked deleterious effects were found in co-exposed mice. At the histomorphological level, crypt depth was increased throughout the intestinal tissues. Significant variations of gene expression related to epithelial, permeability, and inflammatory biomarkers were quantified. Defective recruitment of some intestinal immune cells was observed from the proximal portion of the small intestine to the colon. Several bacterial taxa at the order level were found to be affected by exposure to the MPs by metagenomic analysis of cecal microbiota. These results show that ingestion of PE microbeads induces significant alterations of crucial intestinal markers in mice and underscores the need to further study the health impact of MP exposure in humans.

The development of nanotechnologies is leading to greater abundance of engineered nanoparticles (EN) in the environment, including in the atmospheric air. To date, it has been shown that the most prevalent EN found in the air are silver (Ag), titanium dioxide (TiO

The key role of environmental factors in the pathogenesis of Inflammatory Bowel Diseases (IBD) is recognized. Aluminum is suspected to be a risk factor for IBD. However, mechanisms linking aluminum exposure to disease development are unknown. We examined the role of aluminum transport and subcellular localisation on human colon susceptibility to aluminum-induced inflammation.Human colon biopsies isolated from Crohn's disease (CD) or control patients and Caco-2 cells were incubated with aluminum. The effects of aluminum were evaluated on cytokine secretion and transporter expression. The role of aluminum kinetics parameters was studied in Caco-2 using transport inhibitors and in human colon biopsies by assessing genetic polymorphisms of transporters.Aluminum exposure was shown to induce cytokine secretion in colon of CD but not healthy patients. In Caco-2 cells, aluminum internalisation was correlated with inflammatory status. In human colon, analysis of genetic polymorphisms and expression of ABCB1 and SLC26A3 transporters showed that their decreased activity was involved in aluminum-induced inflammation.We hypothesize that alteration in detoxifying response would lead to a deregulation of intestinal homeostasis and to the expression of IBD. Our study emphasizes the complexity of gene/environment interaction for aluminum adverse health effect, highlighting at risk populations or subtypes of patients. A better understanding of correlations between gene expression or SNP and xenobiotic kinetics parameters would shift the medical paradigm to more personalized disease management and treatment.

International audience; BACKGROUND: Ambient air pollution is recognized as one of the leading causes of global burden of disease. Involvement of air pollution in respiratory and cardiovascular diseases was first recognized, and then cumulative data has indicated that the intestinal tract could be also damaged.OBJECTIVE: To review and discuss the current epidemiological and animal data on the effects of air pollution on intestinal homeostasis.METHODS: An extensive literature search was conducted using Google Scholar and Pubmed to gather relevant human and animal studies that have reported the effects of any air pollutant on the intestine.RESULTS: Exposure to several gaseous and particulate matter components of air pollution have been associated either positively or negatively with the onset of various intestinal diseases including appendicitis, gastroenteric disorders, irritable bowel syndrome, inflammatory bowel diseases, and peptic ulcers. Several atmospheric pollutants have been associated with modifications of gut microbiota in humans. Animal studies have showed that inhalation of atmospheric particulate matter can lead to modifications of gut microbiota, impairments of oxidative and inflammatory intestinal balances, and disruption of gut epithelial permeability.CONCLUSIONS: Overall, the literature appears to indicate that the gut is an underestimated target of adverse health effects induced by air pollution. It is therefore important to develop additional studies that aim to better understand the link between air pollutants and gastro-intestinal diseases.

BACKGROUND: Geographical variations in Crohn's disease (CD) suggest that the environment has a role in the pathogenesis of this condition. OBJECTIVE: To describe the spatial distribution and the clustering of CD cases in France, and to assess the relationship between the prevalence of CD and environmental risk factors. METHODS: We identified all patients with CD included in the French hospital discharge database from 2007 to 2014. Age- and gender-smoothed standardised prevalence ratios over this period were computed for 5610 spatial units. An ecological regression analysis was used to assess the relationship between the risk of CD and ecological variables (health care, latitude, socio-economic deprivation, urbanisation, proportion of agricultural surfaces and density of industries). Local spatial clusters of high-CD prevalence were searched for using elliptic spatial scan statistics and characterised in a hierarchical ascendant classification based on the same ecological variables. RESULTS: About 129 089 patients with CD were identified, yielding a crude prevalence of 203 per 100 000 inhabitants. The overall spatial heterogeneity was statistically significant (P

The Rosa Bonheur research group just published last September 19, in the Amsterdam publishing house, La ville vue d’en bas. Travail et production de l’espace populaire. The book gathers the great results of a long-term ethnographic research carried out between 2011 and 2015 in a pauperized city in northern France. In it, the reader enters into the daily life of men and women who were expelled from wage labor and who have had to organize themselves to meet their most basic subsistence needs as well as those of their families. The ethnographic account, faithful to a French archaeological tradition, is articulated with a pertinent renewal of theoretical and analytical approaches to life and work in deindustrialized spaces. El colectivo de investigación Rosa Bonheur acaba de publicar el 19 de septiembre pasado, en la editorial Amsterdam, La ville vue d’en bas. Travail et production de l’espace populaire El libro recoge los grandes resultados de una investigación etnográfica de largo aliento realizada entre 2011 y 2015 en una ciudad pauperizada del norte de Francia. En él, el lector se adentra en el cotidiano de hombres y mujeres que fueron expulsados del trabajo asalariado y que han debido organizarse para hacer frente a sus necesidades de subsistencia más básicas así como las de sus familias. El relato etnográfico, fiel a una tradición etnográfica francesa, se articula con una pertinente renovación de los planteamientos teóricos y analíticos sobre la vida y el trabajo en los espacios desindustrializados.

Background: Ambient particulate matter (PM) exposure has been shown to increase the risks of respiratory diseases and to contribute to the substantial worldwide burden of respiratory infections. However, the immune response to inhaled PM remains largely unexplored. Aim: We studied the effects of urban coarse PM on the pulmonary immunologic homeostasis. Methods: Male mice were exposed to urban coarse PM in a ventilated inhalation chamber for 3 and 15 days at a concentration relevant to episodic elevation peak of air pollution. Then the characteristics of PM-induced inflammation were assessed by flow cytometry and real-time PCR. Results: Acute and chronic exposures to urban coarse PM led to different immune patterns in the lung compartment. The acute phase was associated to the recruitment of neutrophils and activated alveolar macrophages. The chronic phase was characterized by the influx of activated conventional T cells whereas invariant natural killer T (iNKT) cells were recruited during both phases. Moreover, genes involved in anti-microbial responses, such as Reg3g, Lcn-2, Lyz and Slpi were downregulated in the lungs after acute PM exposure, whereas they were going back to baseline or slightly increased after chronic exposure. Independently of the time course, exposure to PM, leads to a decrease in IL-1b expression. Conclusion: This study provided a characterization of immunologic profiles in lungs following acute and chronic exposure to a realistic dose of PM. It suggested new mechanistic insights which should be further explored, especially the involvement of iNKT cells in pulmonary response to PM inhalation and the effects of PM exposure on the susceptibility to pulmonary infections.

International audience; The mycotoxin deoxynivalenol (DON) is a frequent contaminant of cereals and their by-products in areas with a moderate climate. Produced by Fusarium species, it is one of the most prevalent mycotoxins in cereal crops worldwide, and the most frequently occurring type B trichothecene in Europe. Due to its toxic properties, high stability and prevalence, the presence of DON in the food chain could represent a major public health risk. However, despite its well-known acute toxicological effects, information on the adverse effects of realistic exposure remains limited. We orally exposed mice during 9 months to DON at doses relevant for currently estimated human intake and explored the impact on various gut health parameters. DON exposure induced recruitment of regulatory B cells, and activation of regulatory T cells and dendritic cells in mesenteric lymph nodes. Several inflammatory parameters were increased in colon of DON-exposed mice, whereas inversely inflammatory markers were decreased in ileum. Histomorphological impairments were observed from the duodenum to the colon. Both colon and jejunum presented a hyperproliferation of epithelial cells and an increased expression of mature absorptive cells markers. Finally, DON exposure reshaped gut microbial structure and drastically disturbed the abundance of several bacterial phyla, families, and genera, leading to dysbiosis. Chronic oral exposure to human relevant doses of DON induces several disturbances of gut homeostasis with likely pathological implications for susceptible individuals.

Background Adherent invasive Escherichia coli (AIEC) are suspected to be involved in the pathogenesis of inflammatory bowel diseases. Since AIEC was first described in 1999, despite important progress on its genomic and immune characterizations, some crucial questions remain unanswered, such as whether there exists a natural reservoir, or whether there is asymptomatic carriage. The ECOR collection, including E. coli strains isolated mainly from the gut of healthy humans and animals, constitutes an ideal tool to investigate AIEC prevalence in healthy condition. A total of 61 E. coli strains were examined for characteristics of AIEC. Methods The adhesion, invasion and intramacrophage replication capabilities (AIEC phenotype) of 61 intestinal E. coli strains were determined. The absence of virulence-associated diarrheagenic E. coli pathotypes (EPEC, ETEC, EIEC, EHEC, DAEC, EAEC), and uropathogenic E. coli was checked. Results Out of 61 intestinal strains, 13 (21%) exhibit the AIEC phenotype, 7 are from human origin and 6 are from animal origin. Prevalence of AIEC strains is about 24 and 19% in healthy humans and animals respectively. These strains are highly genetically diverse as they are distributed among the main described phylogroups. Among E. coli strains from the ECOR collection, we also detected strains able to detach I-407 cells. Conclusions Our study described for the first time AIEC strains isolated from the feces of healthy humans and animals.

International audience; Inflammatory Bowel Diseases (IBD) are chronic inflammatory conditions of the intestinal tract. IBD are believed to result from an inappropriate immune response against the intestinal flora in genetically predisposed patients. The precise etiology of these diseases is not fully understood, therefore treatments rely on the dampening of symptoms, essentially inflammation, rather than on the cure of the disease. Despite the availability of biologics, such as anti-TNF antibodies, some patients remain in therapeutic failure and new treatments are thus needed. The multiligand receptor for advanced glycation end-products (RAGE) is a pattern recognition receptor implicated in inflammatory reactions and immune system activation. Here, we investigated the role of RAGE in intestinal inflammation and its potential as a therapeutic target in IBD. We showed that RAGE was upregulated in inflamed tissues from IBD patients compared to controls. Rage(-/-) mice were less susceptible to intestinal and colonic inflammation development than WT mice. WT mice treated with the RAGE-specific inhibitor FPS-ZM1 experienced less severe enteritis and colitis. We demonstrated that RAGE could induce intestinal inflammation by promoting oxidative stress and endothelial activation which were diminished by FPS-ZM1 treatment. Our results revealed the RAGE signaling pathway as a promising therapeutic target for IBD patients.

Cet article est issu d’une enquête ethnographique collective portant sur l’organisation de la vie quotidienne des classes populaires à Roubaix, ville désindustrialisée qui connaît depuis plusieurs décennies un déclin démographique et urbain ainsi qu’un reflux des anciennes dynamiques de valorisation du capital. Les habitants des quartiers pauvres y effectuent des activités telles que la mécanique automobile, qui concerne principalement les hommes. Source de revenus, de qualification et de travail pour différentes générations, la réparation automobile se déploie dans la rue, sur des parkings, dans des garages « à ciel ouvert », plus ou moins clandestins, révélant la porosité de la frontière entre l’informalité et la formalité du travail. Cette activité se réalise au prix d’une plus grande emprise de la division sexuelle et raciale du travail, régulatrice de la distribution des postes et des statuts. Elle s’inscrit, plus largement, dans un système de travail de subsistance que doivent quotidiennement réaliser les hommes et les femmes des classes populaires aux marges du marché du travail formel. L’inscription spatiale de ces pratiques révèle la centralité populaire de Roubaix alors qu’elle est habituellement perçue comme une ville périphérique et reléguée. This article is based upon collective ethnographic fieldwork focusing on the everyday life of the working classes in Roubaix, a de-industrialized city that has been going through demographic and urban decline for several decades while the former processes of capital valorization have been scaled back. The inhabitants of the poorest neighborhoods engage in activities such as auto repairs (in this case, they are essentially men). A source of income, of qualification and of work for different generations, mechanical services are offered in the street, on parking lots or in more or less clandestine “outdoor” garages. They reveal the porosity between formal and informal labor. This activity implies a strong sexual and racial division of labor that regulates the distribution of positions and of status. More generally, it takes place within a wider system of subsistence work in which working class men and women located on the margins of the formal labor market participated daily. The spatial inscription of these practices suggests that Roubaix occupies a central position for this popular economy, while it is usually considered a peripheral and remote city. 216-217;1

Background Air pollution is a recognized aggravating factor for pulmonary diseases and has notably deleterious effects on asthma, bronchitis and pneumonia. Recent studies suggest that air pollution may also cause adverse effects in the gastrointestinal tract. Accumulating experimental evidence shows that immune responses in the pulmonary and intestinal mucosae are closely interrelated, and that gut-lung crosstalk controls pathophysiological processes such as responses to cigarette smoke and influenza virus infection. Our first aim was to collect urban coarse particulate matter (PM) and to characterize them for elemental content, gastric bioaccessibility, and oxidative potential; our second aim was to determine the short-term effects of urban coarse PM inhalation on pulmonary and colonic mucosae in mice, and to test the hypothesis that the well-known antioxidant N-acetyl-L-cysteine (NAC) reverses the effects of PM inhalation. Results The collected PM had classical features of urban particles and possessed oxidative potential partly attributable to their metal fraction. Bioaccessibility study confirmed the high solubility of some metals at the gastric level. Male mice were exposed to urban coarse PM in a ventilated inhalation chamber for 15 days at a concentration relevant to episodic elevation peak of air pollution. Coarse PM inhalation induced systemic oxidative stress, recruited immune cells to the lung, and increased cytokine levels in the lung and colon. Concomitant oral administration of NAC reversed all the observed effects relative to the inhalation of coarse PM. Conclusions Coarse PM-induced low-grade inflammation in the lung and colon is mediated by oxidative stress and deserves more investigation as potentiating factor for inflammatory diseases. Electronic supplementary material The online version of this article (10.1186/s12989-017-0227-z) contains supplementary material, which is available to authorized users.

Fonde sur une enquete qualitative menee aupres de jeunes decohabitants de milieux populaires, cet article analyse le role de la famille dans les processus de decohabitation. On repere trois modeles d'insertion professionnelle et sociale, auxquels correspondent des processus de decohabitation specifiques. Ceux-ci sont souvent orientes par des « roles familiaux de substitution » tenus par les jeunes et dont l'article propose une definition. Essentiellement occupes par des jeunes femmes, ces roles familiaux de substitution circonscrivent leur decohabitation au territoire de la parente et s'averent faiblement emancipateurs.

International audience; Since World War II, several factors such as an impressive industrial growth, an enhanced environmental bioavailability and intensified food consumption have contributed to a significant amplification of human exposure to aluminum. Aluminum is particularly present in food, beverages, some drugs and airbone dust. In our food, aluminum is superimposed via additives and cooking utensils. Therefore, the tolerable intake of aluminum is exceeded for a significant part of the world population, especially in children who are more vulnerable to toxic effects of pollutants than adults. Faced with this oral aluminum influx, intestinal tract is an essential barrier, especially as 38% of ingested aluminum accumulates at the intestinal mucosa. Although still poorly documented to date, the impact of oral exposure to aluminum in conditions relevant to real human exposure appears to be deleterious for gut homeostasis. Aluminum ingestion affects the regulation of the permeability, the microflora and the immune function of intestine. Nowadays, several arguments are consistent with an involvement of aluminum as an environmental risk factor for inflammatory bowel diseases.; Depuis la seconde guerre mondiale, plusieurs facteurs tels qu’un essor industriel impressionnant, une augmentation de la bio-accessibilité environnementale et un accroissement de la consommation alimentaire ont contribué à une amplification importante de l’exposition humaine à l’aluminium. L’aluminium est notamment présent dans la nourriture, les boissons, certains médicaments et dans les poussières atmosphériques. Dans notre alimentation, de l’aluminium se surajoute via les additifs et les ustensiles de cuisine. Par conséquent, la dose tolérable d’aluminium est dépassée pour une part significative de la population mondiale, particulièrement chez les enfants qui sont plus vulnérables aux effets toxiques des polluants que les adultes. Face à cet afflux d’aluminium par voie orale, le tractus intestinal constitue une barrière essentielle, d’autant que 38 % de l’aluminium ingéré s’accumulent au niveau de la muqueuse intestinale. Bien qu’encore peu documenté à ce jour, l’impact de l’exposition orale à l’aluminium en conditions pertinentes par rapport à une exposition humaine réelle semble être délétère pour l’homéostasie de l’intestin. L’ingestion d’aluminium affecte la régulation de la perméabilité, de la microflore et de la fonction immunitaire de l’intestin. De nombreux arguments concordent aujourd’hui vers une implication de l’aluminium en tant que facteur de risque environnemental pour les maladies inflammatoires chroniques de l’intestin.

International audience; Aluminum (Al), a non-essential element, is ubiquitous in industrialized societies. Whereas adult intake is estimated between 3 and 12 mg/day according to dietary aluminum studies conducted in many countries, it is not known if aluminum may have a toxic effect on intestinal epithelium. The aim of this work was to evaluate the cytotoxicity and RNA expression patterns induced in HT-29 cells by aluminum. Both classical toxicological methods and a global transcriptomic approach were used. Cytotoxicity determined by MTT assay showed a time and dose dependent decrease of cell viability in aluminum treated cells compared to control cells. Cell cycle analysis by flow cytometry revealed that aluminum induced accumulation of cells in phase G0/G1, associated with a decrease in the proportion of cells in S and G2/M phases. Aluminum led to apoptosis as evidenced by nuclear morphology changes and mitochondrial membrane perturbations, and induced reactive oxygen species generation. Transcriptomic pattern argued in favor of pro-tumorigenic and pro-inflammatory effects of aluminum in intestinal epithelial cells. These results highlight several pathways by which aluminum has a disturbing impact on intestinal epithelial cells, supporting that the effects of aluminum on intestine warrants further investigation.

Although the heavy metals cadmium (Cd) and lead (Pb) are known environmental health concerns, their long-term impacts on gut ecology and susceptibility to gastrointestinal autoimmune diseases have not been extensively investigated. We sought to determine whether subchronic oral exposure to Cd or Pb is a risk factor for the development and progression of inflammatory bowel disease (IBD). Mice were exposed to various doses of CdCl2 or PbCl2 in drinking water for 1, 4 or 6 weeks prior to infection with Salmonella, the induction of colitis with dextran sodium sulfate (DSS) or trinitrobenzene sulfonic acid (TNBS). In human cell-based models, exposure to Cd and Pb is associated with reduced transepithelial electric resistance and changes in bacteria-induced cytokine responses. Although 1- and 6-week exposures did not have clear effects on the response to Salmonella infectious challenges, 1-week short-term treatments with CdCl2 tended to enhance intestinal inflammation in mice. Unexpectedly, subchronic exposure to Cd and (to a lesser extent) Pb significantly mitigated some of the symptoms of DSS-induced colitis and reduced the severity of TNBS colitis in a dose-dependent manner. The possible adaptive and immunosuppressive mechanisms by which heavy metals might reduce intestinal inflammation are explored and discussed.

International audience

Summary Eukaryotic peptidoglycan recognition proteins (PGRPs) are related to bacterial amidases. In Drosophila , PGRPs bind peptidoglycan and function as central sensors and regulators of the innate immune response. PGRP-LC/PGRP-LE constitute the receptor complex in the immune deficiency (IMD) pathway, which is an innate immune cascade triggered upon Gram-negative bacterial infection. Here, we present the functional analysis of the nonamidase, membrane-associated PGRP-LF. We show that PGRP-LF acts as a specific negative regulator of the IMD pathway. Reduction of PGRP-LF levels, in the absence of infection, is sufficient to trigger IMD pathway activation. Furthermore, normal development is impaired in the absence of functional PGRP-LF, a phenotype mediated by the JNK pathway. Thus, PGRP-LF prevents constitutive activation of both the JNK and the IMD pathways. We propose a model in which PGRP-LF keeps the Drosophila IMD pathway silent by sequestering circulating peptidoglycan.

Inflammatory bowel diseases (IBD) are not rare and would affect near of 5 million of patients in the world (including 2.5 in North America and 2.5 in Europe with at least 200,000 in France). These are chronic relapsing disorders affecting young patients (peak of incidence in patients aged from 20 to 30 years), particularly the young females (sex ratio F/M: 1.3). Their cause is unknown and there is no curative treatment. Although many research studies have isolated more than 160 genes whose variants are associated with these diseases, the weight of genetics remains low in their occurrence. Significant time and space variations in incidence of IBD have been reported. Firstly, an increase of IBD incidence has been reported overtime worldwide. Secondly, a space variation in IBD incidence has been noted with a dramatic increase in emerging countries. Even within a same geographical area through a prospective population-based dataset since 27 years (EPIMAD Registry), a spatial heterogeneity of incidence has been reported, suggesting the important role of the environment in the occurrence of these diseases. Smoking and appendectomy are the only environmental factors clearly involved in the development and progression of IBD and cannot explain spatial and temporal heterogeneity in the IBD observed incidence worldwide. New multidisciplinary basic and epidemiological studies are needed to identify the factors involved in the onset of IBD.

L’objet de l’article est de discuter de methodes d’observation et d’interpretation des arbitrages residentiels de salaries face a la flexibilite de leur emploi. Apres avoir montre les limites de l’investigation quantitative sur cette question, la reflexion s’appuiera sur les resultats d’une enquete qualitative aupres de salaries confrontes, en 2000, a la fermeture de leur usine et a sa delocalisation a 200 km de leur domicile. Dans ce type de situations, ce n’est pas la seule mobilite residentielle suscitee par l’emploi qu’il s’agit d’etudier mais bien les arbitrages entre, a la fois, mobilite et non-mobilite. Cette posture rend ainsi possible l’identification du caractere multidimensionnel de ces choix : les logiques professionnelles n’expliquent pas tout, les logiques familiales et residentielles jouent un role important dans le refus de demenager ou l’amenagement d’un systeme de double residence. Cette approche permet d’apprehender en quoi ces decisions reproduisent, voire aggravent les inegalites sociales, tout en incluant les possibilites de strategies residentielles et spatiales.

Mobilities, Migrations and residential anchorings facing job relocation. The case of a factory closure, in the district of Aisne in Picardy, calling upon employees to relocate two hundred kilometres from their usual place of residence allows us to understand the consequences of the transfer or the dismissal of ivorkers on their mobility. This article points out that it is a system of resources and constraints, partly related to the different types of family configurations in the territory and to the type of tenure, that accounts for choosing “residential anchoring” or definitive migration or even dual residen.ce. These decisions bring in exchange an increased daily home-work commute and weekly or monthly movings towards the family territory. Therefore, the link between ‘residential anchoring’ and daily commute appears unavoidable and reveals unequal social and geographical resources between workers., Le cas de la fermeture d’une usine, dans le département de l’Aisne en Picardie, proposant aux salariés une mutation à deux cents kilomètres de leur domicile permet de comprendre les conséquences de la mutation ou du licenciement sur les mobilités familiales. Les choix de l’ancrage, de la migration définitive ou de la bi-résidentialité relèvent d’un système de ressources et de contraintes en partie lié aux types de configurations familiales dans le territoire d’origine et au statut d'occupation du logement. Ces décisions imposent en contre-partie aux ouvriers et aux techniciens des déplacements quotidiens domicile-travail plus importants, ou bien, des déplacements hebdomadaires ou mensuels vers leur région d’origine. L’articulation entre ancrage résidentiel et déplacements quotidiens s’avère donc nécessaire et révèle les inégalités de ressources sociales et spatiales entre ouvriers., Vignal Cécile. Mobilités, migrations et ancrages face à la délocalisation de l’emploi. In: NETCOM : Réseaux, communication et territoires / Networks and Communication Studies, vol. 19 n°3-4, december 2005. Mobilités familiales. pp. 193-210.

L’objectif du projet TransEnergy financé par l’ANR Villes Durables 2010 était d’apporter des éléments de connaissance sur les stratégies d’adaptation des ménages et des entreprises à la transition énergétique en comparant les choix de localisation des ménages et des entreprises des métropoles de Lille et de Lyon. La recherche, conçue sur une analyse systémique, s’est appuyée sur une analyse des différentes échelles du territoire, des secteurs d’activités industriels et des contraintes des ménages. Elle a été produite grâce à une complémentarité disciplinaire (ont été mobilisées la sociologie, l’anthropologie, l’aménagement et les sciences de l’ingénieur) et des modes d’investigation du réel comprenant l’usage de méthodologies tant quantitatives que qualitatives.

The increasing incidence of inflammatory bowel diseases (IBDs) in developing countries has highlighted the critical role of environmental pollutants as causative factors in their pathophysiology. Despite its ubiquity and immune toxicity, the impact of aluminum in the gut is not known. This study aimed to evaluate the effects of environmentally relevant intoxication with aluminum in murine models of colitis and to explore the underlying mechanisms. Oral administration of aluminum worsened intestinal inflammation in mice with 2,4,6-trinitrobenzene sulfonic acid- and dextran sodium sulfate-induced colitis and chronic colitis in interleukin 10-negative (IL10(-/-)) mice. Aluminum increased the intensity and duration of macroscopic and histologic inflammation, colonic myeloperoxidase activity, inflammatory cytokines expression, and decreased the epithelial cell renewal compared with control animals. Under basal conditions, aluminum impaired intestinal barrier function. In vitro, aluminum induced granuloma formation and synergized with lipopolysaccharide to stimulate inflammatory cytokines expression by epithelial cells. Deleterious effects of aluminum on intestinal inflammation and mucosal repair strongly suggest that aluminum might be an environmental IBD risk factor.

Background: Inflammatory bowel diseases (IBD) patients are abnormally colonized by adherent-invasive Escherichia coli (AIEC). NOD2 gene mutations impair intracellular bacterial clearance. We evaluated the impact of antibiotic treatment on AIEC colonization in wildtype (WT) and NOD2 knockout mice (NOD2KO) and the consequences on intestinal inflammation. Methods: After 3 days of antibiotic treatment, mice were infected for 2 days with 109 CFU AIEC and sacrificed 1, 5, and 60 days later. In parallel, mice were challenged with AIEC subsequent to a dextran sodium sulfate (DSS) treatment and sacrificed 9 days later. Ileum, colon, and mesenteric tissues were sampled for AIEC quantification and evaluation of inflammation. Results: Without antibiotic treatment, AIEC was not able to colonize WT and NOD2KO mice. Compared with nontreated animals, antibiotic treatment led to a significant increase in ileal and colonic colonization of AIEC in WT and/or NOD2KO mice. Persistent AIEC colonization was observed until day 5 only in NOD2KO mice, disappearing at day 60. Mesenteric translocation of AIEC was observed only in NOD2KO mice. No inflammation was observed in WT and NOD2KO mice treated with antibiotics and infected with AIEC. During DSS-induced colitis, colonization and persistence of AIEC was observed in the colon. Moreover, a dramatic increase in clinical, histological, and molecular parameters of colitis was observed in mice infected with AIEC but not with a commensal E. coli strain. Conclusions: Antibiotic treatment was necessary for AIEC colonization of the gut and mesenteric tissues and persistence of AIEC was dependent on NOD2. AIEC exacerbated a preexisting DSS-induced colitis in WT mice. (Inflamm Bowel Dis 2012)

Methods Disruption of commensal microbiota was induced by a 3 days antibiotic treatment orally administered in WT and NOD2KO mice. At day 3, mice were infected with 10 CFU AIEC once a day for 2 days. Animals were sacrificed at day 1, 5, 30 and 60 after AIEC administration. Ileum, colon and mesenteric lymph nodes (MLN) were sampled for AIEC quantification in ileal and colonic tissues, bacterial translocation in MLN, and evaluation of histological abnormalities and intestinal inflammation.

International audience; OBJECTIVE: Yersinia pseudotuberculosis causes ileitis and mesenteric lymphadenitis by mainly invading the Peyer's patches that are positioned in the terminal ileum. Whereas toll-like-receptor 2 (TLR2) controls mucosal inflammation by detecting certain microbiota-derived signals, its exact role in protecting Peyer's patches against bacterial invasion has not been defined. DESIGN: Wild-type, Tlr2-, Nod2- and MyD88-deficient animals were challenged by Y pseudotuberculosis via the oral or systemic route. The role of microbiota in conditioning Peyer's patches against Yersinia through TLR2 was assessed by delivering, ad libitum, exogenous TLR2 agonists in drinking water to germ-free and streptomycin-treated animals. Bacterial eradication from Peyer's patches was measured by using a colony-forming unit assay. Expression of cryptdins and the c-type lectin Reg3 beta was quantified by quantitative reverse transcriptase polymerase chain reaction analysis. RESULTS: Our data demonstrated that Tlr2-deficient mice failed to limit Yersinia dissemination from the Peyer's patches and succumbed to sepsis independently of nucleotide-binding and oligomerisation domain 2 (NOD2). Recognition of both microbiota-derived and myeloid differentiation factor 88 (MyD88)-mediated elicitors was found to be critically involved in gut protection against Yersinia-induced lethality, while TLR2 was dispensable to systemic Yersinia infection. Gene expression analyses revealed that optimal epithelial transcript level of the anti-infective Reg3 beta requires TLR2 activation. Consistently, Yersinia infection triggered TLR2-dependent Reg3 beta expression in Peyer's patches. Importantly, oral treatment with exogenous TLR2 agonists in germ-free animals was able to further enhance Yersinia-induced expression of Reg3 beta and to restore intestinal resistance to Yersinia. Lastly, genetic ablation of Reg3 beta resulted in impaired clearance of the bacterial load in Peyer's patches. CONCLUSIONS: TLR2/REG3 beta is thus an essential component in conditioning epithelial defence signalling pathways against bacterial invasion.

International audience; In mammals, tissue-specific sets of pattern-recognition molecules, including Nod-like receptors (NLR), enable concomitant and sequential detection of microbial-associated molecular patterns from both the extracellular and intracellular microenvironment. Repressing and de-repressing the cytosolic surveillance machinery contributes to vital immune homeostasis and protective responses within specific tissues. Conversely, defective biology of NLR drives the development of recurrent infectious, autoimmune and/or inflammatory diseases by failing to mount barrier functions against pathogens, to tolerate commensals, and/or to instruct the adaptive immune response against microbes. Better decoding microbial strategies that are evolved to circumvent NLR sensing will provide clues for the development of rational therapies aimed at curing and/or preventing common and emerging immunopathologies.

Defensins and cathelicidins are prevalent and essential gastrointestinal cationic antimicrobial peptides (CAPs). However, these defensive peptides are not infallible because certain enteropathogens can overcome their protective function. Furthermore, impaired defensin synthesis has been linked to the occurrence of Crohn's disease (CD), a chronic inflammatory bowel disease. Recently, defective bacterial sensing through NOD1 and NOD2 has been related to reduced defensin production, CD predisposition and susceptibility to enteric infection. Hence, we propose that microbial sensors at the gut interface monitor the levels of these effector peptides, which might function as 'danger' signals to confer tolerance and alert immunocytes. Further work is required to clarify how gastrointestinal CAPs are regulated and to assess their role in maintaining epithelial homeostasis and triggering adaptive immunity.

Si les evenements professionnels creent des ruptures repetees dans la relation entre l’habitat et l’emploi, ils ne conduisent pas systematiquement a un demenagement. Notre objectif est d’identifier les facteurs qui expliquent les comportements de mobilite ou d’ancrage residentiels des salaries touches par l’instabilite de leur emploi ou le chomage. Un cadrage statistique de l’articulation entre mobilite residentielle et emploi, puis de l’articulation entre demenagement et chomage, suggere combien les contraintes professionnelles, residentielles et familiales s’entrecroisent pour expliquer la faible mobilite residentielle des salaries peu qualifies, licencies ou au chomage. Enfin, nous proposons de nouvelles pistes de reflexion forgees a partir d’une approche plus qualitative. La flexibilite de l’emploi et le chomage destabilisent a la fois l’integration professionnelle et les formes de l’integration domestique mais peuvent aussi faire l’objet d’adaptations de la part des salaries.