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Rôle de l'inflammasome NLRP3 dans la destruction parodontale induite par Porphyromonas gingivalis au cours de la parodontite
No full textPeriodontitis is a chronic inflammatory disease initiated by the dysbiosis of oral microbiota. It is characterized by irreversible destruction of the tooth-supporting tissues (e.g., periodontal ligament, cementum, and alveolar bone). Porphyromonas gingivalis is a keystone pathogen implicated in periodontitis that the presence of which leads to the modification of the composition of oral microbiota and the exacerbation of host immune response. Among the inflammatory pathways stimulated by P. gingivalis, NLRP3 inflammasome, an intracellular molecular complex whose activation mediates a release of pro-inflammatory cytokines (IL-1ß, IL-18) into the extracellular environment, as well as the programmed-cell death by pyroptosis. NLRP3 inflammasome is overexpressed in the gingival tissue of periodontitis patients but its role in the pathogenesis of periodontitis remains unclear. The present study aims to better understand the implication of NLRP3 inflammasome in the onset and the development of periodontitis. In this study, a mouse model of periodontitis was used, employing the ligature method, impregnated or not with P. gingivalis, in WT and NLRP3 KO mice. After 28 days of induction, repeated trauma by ligature alone induced an exacerbation of periodontal destruction in KO mice compared to WT mice, with an increase in activated osteoclasts. No significant difference was observed at days 14, suggesting that NLRP3 is protective against alveolar bone loss and involved in regulatory pathways that limit periodontitis. On the other hand, in the presence of P. gingivalis, the protective effect of NLRP3 was not observed. Overexpression of NLRP3 in connective tissue of WT mice increased local production of mature IL'1ß, associated with dramatic mobilization of neutrophils in a bipartite manner between the site of periodontitis induction and the alveolar bone crest. P. gingivalis mediated the targeting of NLRP3-positive neutrophils to the alveolar bone crest, suggesting a role for this subpopulation in periodontal bone loss. However, in NLRP3 KO mice, the expression of mature IL-1ß was lower and almost no neutrophils were recruited to the periodontitis area. In conclusion, our study sheds new light on the protective role of NLRP3 inflammasome in periodontitis and how this role is modulated in neutrophils by P. gingivalis.La parodontite est une maladie inflammatoire chronique initiée par la dysbiose du microbiote buccal. Elle se caractérise par une destruction irréversible des tissus de soutien des dents (e.g., le ligament parodontal, le cément et l'os alvéolaire). Porphyromonas gingivalis est un parodontopathogène impliqué dans la parodontite dont la présence entraîne la modification de la composition du microbiote buccal et l'exacerbation de la réponse immunitaire de l'hôte. Parmi les voies inflammatoires stimulées par P. gingivalis, l'inflammasome NLRP3, un complexe moléculaire intracellulaire dont l'activation induit la maturation et la libération de cytokines pro-inflammatoires (IL-1ß, IL-18) dans le milieu extracellulaire, ainsi que la mort cellulaire programmée par pyroptose. L'inflammasome NLRP3 est surexprimé dans le tissu gingival des patients atteints de parodontite, mais son rôle dans la pathogenèse de la parodontite reste incertain. Dans notre étude, nous utilisons un modèle murin de parodontite, en appliquant la méthode de ligature, imprégnée ou non de P. gingivalis, chez des souris WT et KO NLRP3. Après 28 jours d'induction, des traumatismes répétés par ligature seule ont induit une exacerbation de la destruction parodontale chez les souris KO par rapport aux souris WT, avec une augmentation des ostéoclastes activés. Aucune différence n'a été observée au jour 14, suggérant que NLRP3 est impliqué dans les voies de régulation qui limitent la parodontite. En revanche, en présence de P. gingivalis, l'effet protecteur de NLRP3 n'a pas été observé. La surexpression de NLRP3 dans le tissu conjonctif des souris WT a augmenté la production locale d'IL-1ß mature, associée à une mobilisation spectaculaire des neutrophiles de manière bipartite entre le site d'induction de la parodontite et la crête osseuse alvéolaire. P. gingivalis a déclenché le recrutement des neutrophiles NLRP3-positifs vers la crête osseuse alvéolaire, suggérant un rôle pour cette sous-population dans la perte osseuse parodontale. Cependant, chez les souris KO NLRP3, l'expression de l'IL-1ß mature était plus faible et presque aucun neutrophile n'a été recruté dans la zone de la parodontite. En conclusion, notre étude apporte un nouvel éclairage sur le rôle protecteur de l'inflammasome NLRP3 dans la parodontite et comment ce rôle est modulé dans les neutrophiles par P. gingivalis
Rôle de l'inflammasome NLRP3 dans la destruction parodontale induite par Porphyromonas gingivalis au cours de la parodontite
No full textLa parodontite est une maladie inflammatoire chronique initiée par la dysbiose du microbiote buccal. Elle se caractérise par une destruction irréversible des tissus de soutien des dents (e.g., le ligament parodontal, le cément et l'os alvéolaire). Porphyromonas gingivalis est un parodontopathogène impliqué dans la parodontite dont la présence entraîne la modification de la composition du microbiote buccal et l'exacerbation de la réponse immunitaire de l'hôte. Parmi les voies inflammatoires stimulées par P. gingivalis, l'inflammasome NLRP3, un complexe moléculaire intracellulaire dont l'activation induit la maturation et la libération de cytokines pro-inflammatoires (IL-1ß, IL-18) dans le milieu extracellulaire, ainsi que la mort cellulaire programmée par pyroptose. L'inflammasome NLRP3 est surexprimé dans le tissu gingival des patients atteints de parodontite, mais son rôle dans la pathogenèse de la parodontite reste incertain. Dans notre étude, nous utilisons un modèle murin de parodontite, en appliquant la méthode de ligature, imprégnée ou non de P. gingivalis, chez des souris WT et KO NLRP3. Après 28 jours d'induction, des traumatismes répétés par ligature seule ont induit une exacerbation de la destruction parodontale chez les souris KO par rapport aux souris WT, avec une augmentation des ostéoclastes activés. Aucune différence n'a été observée au jour 14, suggérant que NLRP3 est impliqué dans les voies de régulation qui limitent la parodontite. En revanche, en présence de P. gingivalis, l'effet protecteur de NLRP3 n'a pas été observé. La surexpression de NLRP3 dans le tissu conjonctif des souris WT a augmenté la production locale d'IL-1ß mature, associée à une mobilisation spectaculaire des neutrophiles de manière bipartite entre le site d'induction de la parodontite et la crête osseuse alvéolaire. P. gingivalis a déclenché le recrutement des neutrophiles NLRP3-positifs vers la crête osseuse alvéolaire, suggérant un rôle pour cette sous-population dans la perte osseuse parodontale. Cependant, chez les souris KO NLRP3, l'expression de l'IL-1ß mature était plus faible et presque aucun neutrophile n'a été recruté dans la zone de la parodontite. En conclusion, notre étude apporte un nouvel éclairage sur le rôle protecteur de l'inflammasome NLRP3 dans la parodontite et comment ce rôle est modulé dans les neutrophiles par P. gingivalis.Periodontitis is a chronic inflammatory disease initiated by the dysbiosis of oral microbiota. It is characterized by irreversible destruction of the tooth-supporting tissues (e.g., periodontal ligament, cementum, and alveolar bone). Porphyromonas gingivalis is a keystone pathogen implicated in periodontitis that the presence of which leads to the modification of the composition of oral microbiota and the exacerbation of host immune response. Among the inflammatory pathways stimulated by P. gingivalis, NLRP3 inflammasome, an intracellular molecular complex whose activation mediates a release of pro-inflammatory cytokines (IL-1ß, IL-18) into the extracellular environment, as well as the programmed-cell death by pyroptosis. NLRP3 inflammasome is overexpressed in the gingival tissue of periodontitis patients but its role in the pathogenesis of periodontitis remains unclear. The present study aims to better understand the implication of NLRP3 inflammasome in the onset and the development of periodontitis. In this study, a mouse model of periodontitis was used, employing the ligature method, impregnated or not with P. gingivalis, in WT and NLRP3 KO mice. After 28 days of induction, repeated trauma by ligature alone induced an exacerbation of periodontal destruction in KO mice compared to WT mice, with an increase in activated osteoclasts. No significant difference was observed at days 14, suggesting that NLRP3 is protective against alveolar bone loss and involved in regulatory pathways that limit periodontitis. On the other hand, in the presence of P. gingivalis, the protective effect of NLRP3 was not observed. Overexpression of NLRP3 in connective tissue of WT mice increased local production of mature IL'1ß, associated with dramatic mobilization of neutrophils in a bipartite manner between the site of periodontitis induction and the alveolar bone crest. P. gingivalis mediated the targeting of NLRP3-positive neutrophils to the alveolar bone crest, suggesting a role for this subpopulation in periodontal bone loss. However, in NLRP3 KO mice, the expression of mature IL-1ß was lower and almost no neutrophils were recruited to the periodontitis area. In conclusion, our study sheds new light on the protective role of NLRP3 inflammasome in periodontitis and how this role is modulated in neutrophils by P. gingivalis
Going Beyond Counting First Authors in Author Co-citation Analysis
Get PDFThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
Variations on the Author
Get PDF“Variations on the Author” discusses two of Eduardo Coutinho’s recent films (Um Dia na Vida, from 2010, and Últimas Conversas, posthumously released in 2015) and their contribution to the general question of documentary authorship. The director’s filmography is characterized by a consistent yet self-effacing form of authorial self-inscription: Coutinho often features as an interviewer that rather than express opinions propels discourses; an interviewer that is good at listening. This mode of self-inscription characterizes him as an author who is not expressive but who is nonetheless markedly present on the screen. In Um Dia na Vida, however, Coutinho is completely absent form the image, while Últimas Conversas, on the contrary, includes a confessional prologue that moves the director from the margins to the center of his films. This article examines the ways in which these works stand out in the filmography of a director who offers new insights into the notion of cinematic authorship
Appropriate Similarity Measures for Author Cocitation Analysis
Get PDFWe provide a number of new insights into the methodological discussion about author cocitation analysis. We first argue that the use of the Pearson correlation for measuring the similarity between authors’ cocitation profiles is not very satisfactory. We then discuss what kind of similarity measures may be used as an alternative to the Pearson correlation. We consider three similarity measures in particular. One is the well-known cosine. The other two similarity measures have not been used before in the bibliometric literature. Finally, we show by means of an example that our findings have a high practical relevance.information science;Pearson correlation;cosine;similarity measure;author cocitation analysis
Dispelling the Myths Behind First-author Citation Counts
Get PDFWe conducted a full-scale evaluative citation analysis study of scholars in the XML research field to explore just how different from each other author rankings resulting from different citation counting methods actually are, and to demonstrate the capability of emerging data and tools on the Web in supporting more realistic citation counting methods. Our results contest some common arguments for the continued
use of first-author citation counts in the evaluation of scholars, such as high correlations between author rankings by first-author citation counts and other citation
counting methods, and high costs of using more realistic citation counting methods that are not well-supported by the ISI databases. It is argued that increasingly available digital full text research papers make it possible for citation analysis studies to go beyond what the ISI databases have directly supported and to employ more
sophisticated methods
koamabayili/VECTRON-author-checklist: VECTRON author checklist
No full textWe have done our best to complete the author checklist relating to the use of animals in the hut study. Note that the objective for the hut study was to evaluate the IRS treatment applications for residual efficacy against Anopheles mosquitoes, including the local An. coluzzii mosquito population. Cows were only used to attract mosquitoes into the huts and no tests were carried out directly on the cows. The author checklist is intended for use with studies where experiments are carried out on animals, which is why we have had such difficulty in completing this for the hut study, as many of the questions do not relate to how the cows were used
Author-wise bibliometric analysis based on entropy.
No full textAuthor-wise bibliometric analysis based on entropy.</p
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