{"title":"Hypermutability and homeologous recombination: Ingredients for rapid evolution","authors":"T.A. Cebula, J.E. LeClerc","doi":"10.1016/S0020-2452(97)83917-6","DOIUrl":"10.1016/S0020-2452(97)83917-6","url":null,"abstract":"<div><p>We examine basic tenets of evolution, i.e., the relative roles that mutation and recombination play in instituting the genetic diversity upon which selection works to establish bacteria in particular niches. Specifically, we delve into the importance of particular mutator phenotypes and their potential contributions to homeologous recombination in bacteria. The implications for rapid evolution and the emergence of new pathogens are discussed.</p></div><div><p>Nous examinons la nature des clones bactériens et les rôles relatifs joués par la mutation et la recombinaison dans la mise en place de la diversité génétique des espèces bactériennes. Établissant, à partir de la volumineuse littérature existant sur <em>Escherichia coli</em> et <em>Salmonella typhimurium</em>, les paradigmes bactériens des transactions de l'ADN, nous trouvons que la question de la fréquence ou de la rareté des événements de recombinaison intra-espèce est non résolue. Nous discutons ici, le fait que des bactéries isolées, <em>E. coli</em> et <em>Salmonella enterica</em> pathogènes prises individuellement, présentent des fréquences de mutation en excès de l'ordre de 1000 fois par rapport à celles de leurs contemporaines. Comme ces isolats sont défectifs pour la réparation des erreurs méthyle-dirigées, principale garantie contre les transferts d' ADN inter-espèces, nous suggérons que les phénotypes hypermutant et hyperecombinant de ces isolats pourraient jouer un rôle dans l'émergence rapide (évolution) de souches pathogènes spécifiques.</p></div>","PeriodicalId":89103,"journal":{"name":"Bulletin de l'Institut Pasteur","volume":"95 2","pages":"Pages 97-106"},"PeriodicalIF":0.0,"publicationDate":"1997-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0020-2452(97)83917-6","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"55825461","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
A.M. Cooper , B.M. Saunders , C.D. D'Souza , A.A. Frank , I.M. Orme
{"title":"Mycobacterium tuberculosis-driven processes in gene-disrupted mice","authors":"A.M. Cooper , B.M. Saunders , C.D. D'Souza , A.A. Frank , I.M. Orme","doi":"10.1016/S0020-2452(97)83916-4","DOIUrl":"10.1016/S0020-2452(97)83916-4","url":null,"abstract":"<div><p>Mice which have disrupted genes for important components of the immune system have been used to study the role of these components in the immune response to infection with <em>Mycobacterium tuberculosis</em>. This has resulted in the identification of interleukin-12 (IL12), interferon-γ (IFNγ), tumour necrosis factor-α (TNFα) and inducible nitric oxide synthase (iNOS) as being essential to the protective response. Less crucial but perhaps more intriguing roles for other molecules such as intercellular adhesion molecule (ICAM) and IL6 have also been suggested by this kind of analysis.</p></div><div><p>L'utilisation de souris génétiquement modifiées a apporté de nouveaux éclairages sur la question de savoir comment les différents éléments immunologiques protègent leur hôte mammifère contre les maladies infectieuses. Cette revue rassemble les observations des diverses équipes de recherche qui utilisent des souris génétiquement modifiées pour l'étude des réponses à l'infection par <em>Mycobacterium tuberculosis</em>.</p><p>Des études antérieures de cette infection chez des souris immunocompétentes avaient suggéré le rôle protecteur joué par l'IFNγ (interféron-γ), le TNFα (tumour necrosis factor α), l'IL12 (interleukine-12) et l'iNOS (inducible nitric oxide synthase). L'infection des souris dont les genes pour ces molécules ont été modifiés a confirmé l'importance capitale de chacun de ces éléments dans la réponse immunitaire protectrice contre la tuberculose. Les informations recueillies dans l'étude de ces souris suggèrent que l'INFγ et le TNFα sont les principaux médiateurs de l'activation des macrophages et que le mécanisme essentiel du contrôle bactérien est la production d'oxyde nitrique par l'iNOS. Étant donné que la production naturelle d'INFγ est insuffisante pour contrôler l'infection par <em>M. tuberculosis</em> chez la souris, l'augmentation de la production d'INFγ est nécessaire. Les cellules responsables de cet accroissement sont les lymphocytes T et, de fait, la mort rapide des souris déficientes en cellules Tαβ, infectées par <em>M. tuberculosis</em>, a confirmé cette observation. L'augmentation des cellules T productrices d'INFγ étudiée dans des systèmes modèles est dépendante de l'IL12, et l'absence de cellules T activées productrices d'INFγ chez la souris déficiente en IL12 a confirmé l'existence de ce processus au cours de l'infection par <em>M. tuberculosis</em>.</p><p>Bien que les cellules T CD4 soient impliquées en tant que principale sous-population protectrice, le rôle des cellules T CD8 dans l'immunité pulmonaire a toujours été sous-entendu. La question de savoir si ce rôle est médié par la production de cytokines ou par la lyse des cellules infectées, a été éclairée par l'absence d'une quelconque difference, au cours de l'infection, entre les souris témoins et les souris déficientes en mécanismes lytiques ordinaires.</p><p>La nature de la réponse inflammatoire pulmonaire connaît un regain d'intérêt, et l'utilisation ","PeriodicalId":89103,"journal":{"name":"Bulletin de l'Institut Pasteur","volume":"95 2","pages":"Pages 85-96"},"PeriodicalIF":0.0,"publicationDate":"1997-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0020-2452(97)83916-4","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"55825324","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Are heart attacks infectious? A critical look at the link between Chlamydia pneumoniae and atherosclerosis","authors":"S.M. Weiss , M.R. Hammerschlag","doi":"10.1016/S0020-2452(97)83918-8","DOIUrl":"10.1016/S0020-2452(97)83918-8","url":null,"abstract":"<div><p><em>Chlamydia pneumoniae</em> is a common cause of respiratory tract infections, and recent evidence suggests that it may also contribute to atherosclerosis. This review evaluates the literature to date and proposes further research to determine if there is in fact a cause and effect relationship between <em>C. pneumoniae</em> infection and atherosclerosis.</p></div><div><p><em>Chlamydia pneumoniae</em>, agent pathogène respiratoire caractérisé pour la premiere fois en 1986, est maintenant reconnue comme cause courante de l'infection des voies respiratoires hautes et basses dans une collectivité donnée. De plus, les preuves s'accumulent dans la littérature scientifique suggérant que <em>C. pneumoniae</em> peut contribuer au développement de l'athérosclérose. Cette conviction est basée sur les études sérologiques et histologiques chez l'homme, sur les études de <em>C. pneumoniae in vitro</em> et sur les investigations faites chez les animaux. Toutefois la littérature moderne s'appuie plutôt sur les corrélations statistiques et les données de l'observation que sur des investigations rigoureuses pour établir une relation étiologique. Les postulats de Koch ne sont pas encore satisfaits, et <em>C. pneumoniae</em> n'est pas universellement acceptée comme une cause de l'athéroscérose. Dans cette revue sont examinées les forces et les faiblesses de la littérature moderne, et sont explorées les possibilités de recherches ultérieures sur le sujet.</p></div>","PeriodicalId":89103,"journal":{"name":"Bulletin de l'Institut Pasteur","volume":"95 2","pages":"Pages 107-113"},"PeriodicalIF":0.0,"publicationDate":"1997-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0020-2452(97)83918-8","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"55825560","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"VIe Symposium international de la société européenne de biochromatographie (esbc)","authors":"","doi":"10.1016/S0020-2452(97)82549-3","DOIUrl":"https://doi.org/10.1016/S0020-2452(97)82549-3","url":null,"abstract":"","PeriodicalId":89103,"journal":{"name":"Bulletin de l'Institut Pasteur","volume":"95 1","pages":"Page 3"},"PeriodicalIF":0.0,"publicationDate":"1997-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0020-2452(97)82549-3","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"136508625","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"XIe Congrès de la société européenne d'immunologie et d'hématologie pédiatriques 14–17 mai 1997, Thessalonique (Grèce)","authors":"","doi":"10.1016/S0020-2452(97)82550-X","DOIUrl":"https://doi.org/10.1016/S0020-2452(97)82550-X","url":null,"abstract":"","PeriodicalId":89103,"journal":{"name":"Bulletin de l'Institut Pasteur","volume":"95 1","pages":"Page 3"},"PeriodicalIF":0.0,"publicationDate":"1997-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0020-2452(97)82550-X","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"136508626","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Le rétrocontrôle négatif de l'inflammation: rôle des cytokines antiinflammatoires","authors":"C. Marie, J.-M. Cavaillon","doi":"10.1016/S0020-2452(97)82541-9","DOIUrl":"10.1016/S0020-2452(97)82541-9","url":null,"abstract":"<div><p>Transforming growth factor-β (TGFβ), interferon-α (IFNα), interleukin-4 (IL4), IL10 and IL13 have the capacity for inhibiting the production of inflammatory cvtokines such as IL1, IL6, tumour necrosis factor (TNFα), IL8 and the other chemokines. Consequently, these cytokines have been designated antimflammatory cytokines. In addition, they can counteract the proinflammatory activities of IL1 and TNF, such as tissue factor induction involved in coagulation, or the expression of adhesion molecules on the endothelial cell surface. Furthermore, IL4, IL10, IL13, TGFβ and IFNα can induce the production of IL1 receptor antagonists (IL1ra) which specifically limit the activity of IL1. The main natural inhibitors of TNF are the soluble TNF receptors, the release of which is enhanced during inflammation. Corticoids also repress the production of proinflammatory cytokines but do not affect or even enhance the production of antimflammatory cytokines. IL6, as the main inducer of acute phase protein synthesis, can be considered an antiinflammatory cytokine. However, all proinflammatory producing cells are not similarly sensitive to the effects of antiinflammatory cytokines. In addition, the nature and sequence of messages acting on the target cell may modify its reactivity to the negative signals delivered by the antiinflammatory cytokines. Finally, wide individual heterogeneity amplifies the diversity of the inflammatory responses. Thus, the world of cytokines is a complex one, and the nature of signals and of responding cells as well as the sequences of events are the unique characteristics of an inflammatory process induced by infectious and non-infectious stimuli.</p></div>","PeriodicalId":89103,"journal":{"name":"Bulletin de l'Institut Pasteur","volume":"95 1","pages":"Pages 41-54"},"PeriodicalIF":0.0,"publicationDate":"1997-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0020-2452(97)82541-9","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"55824760","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"IIe Colloque des 3r: réplication, recombinaison et réparation","authors":"","doi":"10.1016/S0020-2452(97)82558-4","DOIUrl":"https://doi.org/10.1016/S0020-2452(97)82558-4","url":null,"abstract":"","PeriodicalId":89103,"journal":{"name":"Bulletin de l'Institut Pasteur","volume":"95 1","pages":"Page 5"},"PeriodicalIF":0.0,"publicationDate":"1997-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0020-2452(97)82558-4","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"136517644","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"VIe Colloque sur le contrôle épidémiologique des maladies infectieuses","authors":"","doi":"10.1016/S0020-2452(97)82555-9","DOIUrl":"https://doi.org/10.1016/S0020-2452(97)82555-9","url":null,"abstract":"","PeriodicalId":89103,"journal":{"name":"Bulletin de l'Institut Pasteur","volume":"95 1","pages":"Page 4"},"PeriodicalIF":0.0,"publicationDate":"1997-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0020-2452(97)82555-9","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"136517646","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"VIe conférence annuelle ibc sur la maladie d'alzheimer","authors":"","doi":"10.1016/S0020-2452(97)82545-6","DOIUrl":"https://doi.org/10.1016/S0020-2452(97)82545-6","url":null,"abstract":"","PeriodicalId":89103,"journal":{"name":"Bulletin de l'Institut Pasteur","volume":"95 1","pages":"Page 2"},"PeriodicalIF":0.0,"publicationDate":"1997-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0020-2452(97)82545-6","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"137195731","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}