Collaboration scientifique et échanges Acadie-Québec : Rétrospectives et projets actuels

Les auteures de ce texte font le bilan de cinquante ans de collaboration entre les folkloristes, ethnographes et ethnologues de l’Acadie et du Québec. Les rencontres et les échanges qui ont autrefois stimulé l’intérêt de différents chercheurs pour de nouveaux objets d’étude et pour de nouvelles approches permettent aujourd’hui la conduite de travaux à caractère comparatif entre les deux régions. Elles retracent le développement des échanges dans le domaine de la recherche et de l’enseignement, de même que l’apport des différents chercheurs depuis les pionniers jusqu’aux ethnologues d’aujourd’hui. Les auteures font également le point sur le contexte actuel des collaborations et proposent quelques avenues susceptibles de favoriser une collaboration accrue entre les deux communautés scientifiques.The authors of this text provide an account of 50 years of collaboration between folklorists, ethnographers and ethnologists from Acadia and Quebec. The meetings and exchanges which once sparked interest among various researchers in new objects of study and new approaches now make possible the transmission of work of a comparative nature between the two regions. The authors trace the development of exchanges in the area of teaching and research, as well as the contribution of various researchers, from early pioneers to contemporary ethnologists. They also take stock of the present-day context in which collaborations are taking place and suggest several ways of fostering an increased collaboration between the two scientific communities

La question des échelles en sciences humaines et sociales

Le double mouvement de globalisation et de localisation des phénomènes sociodémographiques a donné une acuité inédite à la question des échelles en sciences humaines et sociales, renouvelant les questions d’articulation entre les niveaux micro et macro. Dans le même temps, le décloisonnement des pratiques scientifiques n’a cessé d’encourager les chercheurs à revoir et à partager leurs échelles d’observation et d’analyse. Changer d’échelle, qu’elle soit spatiale, temporelle ou catégorielle, c’est adopter une autre optique sur un même objet de recherche mais cela ne se fait pas sans risques. Encore trop souvent reléguée à une dimension technique, il s’agit pourtant d’une question des plus fécondes pour sans cesse réinterroger collectivement les dynamiques des sociétés contemporaines. Les auteurs de cet ouvrage – géographes, sociologues, anthropologues, démographes – relèvent ces défis épistémologiques et méthodologiques à partir de leurs pratiques de recherche sur des terrains aussi variés que l’Afrique de l’Ouest et du Nord, le Moyen-Orient, l’Asie du Sud-Est, la Mélanésie ou encore l’Europe

Interleukin-33 and RANK-L Interplay in the Alveolar Bone Loss Associated to Periodontitis.

Chronic Periodontitis (CP) is an inflammatory disease of bacterial origin that results in alveolar bone destruction. Porphyromonas gingivalis (Pg), one of the main periopathogens, initiates an inflammatory cascade by host immune cells thereby increasing recruitment and activity of osteoclasts, the bone resorbing cells, through enhanced production of the crucial osteoclastogenic factor, RANK-L. Antibodies directed against some cytokines (IL-1β, IL-6 and TNF-α) failed to exhibit convincing therapeutic effect in CP. It has been suggested that IL-33, could be of interest in CP.the present study aims to analyze whether and how IL-33 and RANK-L and/or their interplay are involved in the bone destruction associated to CP.mRNAs and protein expressions of IL-33 and RANK-L were analyzed in healthy and CP human gingival samples by immunohistochemistry (IHC) and RT-qPCR. Murine experimental periodontitis (EP) was induced using Pg infected ligature and Pg free ligature around the first maxillary molar. Alveolar bone loss was recorded by μCT. Mouse gingival explants were stimulated for 24 hours with IL-33 and RANK-L mRNA expression investigated by RT-qPCR. Human oral epithelial cells were infected by Pg for 6, 12; 24 hours and IL-33 and RANK-L mRNA expressions were analyzed by RT-qPCR.IL-33 is overexpressed in gingival epithelial cells in human affected by CP as in the murine EP. In human as in murine gingival cells, RANK-L was independently induced by Pg and IL-33. We also showed that the Pg-dependent RANK-L expression in gingival epithelial cells occured earlier than that of IL-33.Our results evidence that IL-33 overexpression in gingival epithelial cells is associated with CP and may trigger RANK-L expression in addition to a direct effect of Pg. Finally, IL-33 may act as an extracellular alarmin (danger signal) showing proinflammatory properties in CP perpetuating bone resorption induced by Pg infection

A tumor-specific mechanism of Treg enrichment mediated by the integrin αvβ8

Regulatory T cells (Tregs) that promote tumor immune evasion are enriched in certain tumors and correlate with poor prognosis. However, mechanisms for Treg enrichment remain incompletely understood. We described a mechanism for Treg enrichment in mouse and human tumors mediated by the αvβ8 integrin. Tumor cell αvβ8 bound to latent transforming growth factor-β (L-TGF-β) presented on the surface of T cells, resulting in TGF-β activation and immunosuppressive Treg differentiation in vitro. In vivo, tumor cell αvβ8 expression correlated with Treg enrichment, immunosuppressive Treg gene expression, and increased tumor growth, which was reduced in mice by αvβ8 inhibition or Treg depletion. Structural modeling and cell-based studies suggested a highly geometrically constrained complex forming between αvβ8-expressing tumor cells and L-TGF-β-expressing T cells, facilitating TGF-β activation, independent of release and diffusion, and providing limited access to TGF-β inhibitors. These findings suggest a highly localized tumor-specific mechanism for Treg enrichment

Time-course of alveolar bone loss in the ligature-induced murine model of experimental periodontitis.

<p>CD1 Swiss mice (n = 90) were subjected to experimental periodontitis for 4, 14 and 28 days. At each time point, animals were sacrificed and maxillary samples were harvested. A. After 4, 14 and 28 days, μCT analysis was performed. Longitudinal sections through the middle of the palatal root of the first maxillary molar (left images) and transversal sections from the apices of the three roots of the first maxillary molar to the summit of the alveolar bone crest (right images) are presented for each time points. B. Alveolar bone loss was assessed using 2D μCT. At each time point, data of ligatured groups (Lig and <i>Pg</i> L) were compared to their respective Sham groups. Data are shown as means ± SEM. * p<0.05.</p

Characteristics of the patients.

<p>Characteristics of the patients.</p

Characterization of human gingival samples in healthy and patients affected by chronic periodontitis.

<p>A. Samples were stained for the T lymphocytes marker CD3 (arrows). Sections were counterstained with Harris Hematoxylin staining. EP: Epithelium; CT: Connective Tissue. B. TNF-α and IL-6 expression in healthy and CP patients were measured by RT-qPCR. Data are shown as mean ± SD. Healthy samples n = 9; chronic periodontitis samples n = 13. Bar = 250μm. *p<0.05, **p<0.01.</p

<i>Pg</i> infection increased the expression of RANK-L and IL-33 mRNAs in human oral epithelial cells.

<p>Human oral epithelial cells (OKF6/TERT2) were cultured with <i>Pg</i> at 10:1 or 100:1 MOI for 6, 12 or 24 hours. mRNAs encoding for IL-33 (A) and RANK-L ((B) were quantified by RT-qPCR. Three separate sets of experiment were performed. Data are shown as mean ± SEM. *p<0.05; **p<0.01.</p