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18 février 2012 6 18 /02 /février /2012 12:29
Des antibiotiques contre l'Autisme Pr Montagnier Le Monde

http://www.afg-web.fr/IMG/pdf/Le_Monde_2010-12-11.pdf
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18 février 2012 6 18 /02 /février /2012 12:20
Luc Montagnier, Nobel de médecine, veut lancer un essai fondé sur la prise prolongée d’anti-infectieux, en s’appuyant sur l’hypothèse controversée de la mémoire de l’eau. L’information a été dévoilée, jeudi 9 décembre, par Declan Butler, journaliste chevronné de l’hebdomadaire scientifique britannique Nature : le professeur Luc Montagnier projette de réaliser en France un essai clinique afin d’évaluer les effets bénéfiques possibles de la prise prolongée d’antibiotiques chez des enfants autistes. Cette expérimentation laisse perplexes des spécialistes de l’autisme. Luc Montagnier, co-lauréat du prix Nobel de médecine en 2008 pour la découverte du virus du SIDA, devrait utiliser, a côté de techniques biologiques classiques, des procédés qui évoquent la théorie très controversée de la « mémoire de l’eau ». Proposée en 1988 par le professeur Jacques Benveniste, elle supposait que l’eau garde une mémoire des substances qu’elle avait contenues, alors que des dilutions avaient fait disparaitre ces substances de la solution aqueuse. L’entourage du professeur Montagnier confirme ce projet, qui n’a pas encore été soumis à l’approbation d’un comité d’éthique. L’essai pilote rechercherait, selon Nature, la trace d’infections chez 30 enfants autistes, ainsi que chez une vingtaine d’enfants indemnes, à des fins de comparaison. Les enfants prendraient ensuite des antibiotiques pendant plusieurs mois et leur évolution serait évaluée. Afin de mener à bien ces travaux, Luc Montagnier bénéficierait d’un financement de plus de 30 000 euros de la part de l’Autism Research Institute, basé à San Diego (Californie). Cf article du Monde ci-joint en date du 11 décembre 2010 : Le Monde édition du 11 décembre 2010 en pdf Ces théories sont très controversées mais le sont encore plus celles fondées sur la prise de vitamines et l’application absurde de régimes alimentaires pour traiter l’autisme et non pour des troubles associés distincts et spécifiques. Là aussi, un circuit parallèle s’installe, souvent bien juteux, profitant du désespoir des familles touchées par le handicap.
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18 février 2012 6 18 /02 /février /2012 08:04
M cell-depletion blocks oral prion disease pathogenesis Mucosal Immunology (2012) 5, 216–225; doi:10.1038/mi.2011.68; published online 1 February 2012 D S Donaldson1,6, A Kobayashi1,2,6, H Ohno3, H Yagita4, I R Williams5 and N A Mabbott1 1The Roslin Institute and Royal (Dick) School of Veterinary Sciences, University of Edinburgh, Edinburgh, UK 2Tohoku University Graduate School of Medicine, Sendai, Japan 3Research Center for Allergy and Immunology, RIKEN, Suehiro, Yokohama, Japan 4Department of Immunology, Juntendo University School of Medicine, Tokyo, Japan 5Department of Pathology, Emory University School of Medicine, Atlanta, Georgia, USA 6These authors contributed equally to this work Correspondence: NA Mabbott, (neil.mabbott@roslin.ed.ac.uk) Received 4 November 2011; Accepted 19 December 2011; Published online 1 February 2012. Abstract Many prion diseases are orally acquired. Our data show that after oral exposure, early prion replication upon follicular dendritic cells (FDC) in Peyer's patches is obligatory for the efficient spread of disease to the brain (termed neuroinvasion). For prions to replicate on FDC within Peyer's patches after ingestion of a contaminated meal, they must first cross the gut epithelium. However, the mechanism through which prions are conveyed into Peyer's patches is uncertain. Within the follicle-associated epithelium overlying Peyer's patches are microfold cells (M cells), unique epithelial cells specialized for the transcytosis of particles. We show that following M cell-depletion, early prion accumulation upon FDC in Peyer's patches is blocked. Furthermore, in the absence of M cells at the time of oral exposure, neuroinvasion and disease development are likewise blocked. These data suggest M cells are important sites of prion uptake from the gut lumen into Peyer's patches.
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18 février 2012 6 18 /02 /février /2012 07:58
Periodontitis, Porphyromonas, and the pathogenesis of rheumatoid arthritis Mucosal Immunology (2012) 5, 112–120; doi:doi:10.1038/mi.2011.66; published online 25 January 2012 D Farquharson1, J P Butcher2 and S Culshaw1 1Infection and Immunity Research Group, University of Glasgow Dental School, School of Medicine, Glasgow, UK 2Division of Infection, Immunity and Inflammation, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, UK Correspondence: S Culshaw, (shauna.culshaw@glasgow.ac.uk) Received 7 November 2011; Accepted 19 December 2011; Published online 25 January 2012. Abstract Epidemiological data indicate a link between rheumatoid arthritis (RA) and periodontal disease (PD). In vitro and in vivo studies have sought to dissect potential mechanisms by which PD may contribute to initiation and progression of RA. However, these are both multifactorial, chronic diseases, and their complex etiologies and pathogenesis themselves remain incompletely understood. Could there really be an etiological link or does this simply represent a statistical coincidence muddied by common risk factors? This review seeks to provide background on these two diseases in the context of recent discoveries suggesting that their pathogenesis may be related. In particular, the process of citrullination, a post-translational protein modification, has been highlighted as a process common to both diseases. The evidence for a relationship between the diseases is explored and its potential mechanisms discussed.
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17 février 2012 5 17 /02 /février /2012 20:14
2011 a été une année d’espoir pour la lutte contre le paludisme, avec le bilan très encourageant publié dans le rapport du Partenariat Roll Back Malaria (Faire Reculer le Paludisme), auquel s’ajoutent les résultats prometteurs d'un essai de vaccination à grande échelle de phase III par le vaccin RTS,S de GlaxoSmithKline. Dans Trends in Parasitology, M B Markus souligne les lacunes qui persistent dans notre connaissance des formes parasitaires quiescentes ou latentes qui représentent une difficulté supplémentaire pour l’éradication du paludisme. Les hypnozoïtes sont des formes quiescentes intra-hépatocytaires responsables des accès de reviviscence qui peuvent survenir après des mois ou des années dans les infections à Plasmodium vivax. Il est très vraisemblable que les hypnozoïtes dérivent directement des sporozoïtes inoculés par le moustique et non de mérozoïtes issus de la division schizogonique hépatique ou érythrocytaire. Si l’hypothèse était avérée, le risque de réactivation des hypnozoïtes pourrait être supprimé en ciblant les stades sporozoïte ou post-sporozoïte mais ce point important reste à prouver. Le seul antipaludéen actuellement actif contre les hypnozoïtes est la primaquine, une amino-8-quinoléine qui induit une hémolyse chez les patients déficients en G6PD et ne peut être utilisé en traitement de masse. L’existence d’hypnozoïtes génétiquement différents chez les individus infectés pose également un problème pour le développement d’un vaccin contre P. vivax. Une protection vaccinale initialement efficace sur les stades de multiplication hépatique primaire pourrait se montrer par la suite inefficiente lors de l’activation plus ou moins tardive des hypnozoïtes résiduels. Des rechutes à long terme peuvent s’observer après plus de 50 ans dans la fièvre quarte due à P. malariae et au moins après 10 ans dans les infections à P. falciparum. Pour ces 2 espèces il est admis qu’il n’existe pas d’hypnozoïtes, et si la baisse progressive de l’état de semi-immunité peut expliquer les rechutes à court terme cela n’est pas le cas pour les réactivations très tardives. L’hypothèse la plus vraisemblable est que ces rechutes tardives sont dues à des mérozoïtes latents ayant échappé à la réponse immunitaire, qui pourraient être localisés au sein des cellules spléniques. Ces parasites latents sont aussi probablement la source de certains accès de reviviscence observés chez P. vivax dans lesquels les parasites ont un génotype identique au génotype initial. Hypnozoïtes ou mérozoïtes latents, l’existence de ces parasites en sommeil au métabolisme réduit et capables d’échapper à la réaction immunitaire devra être prise en compte pour le développement de médicaments ou de vaccins antipaludéens efficaces à long terme. Dr JF Garin Markus MB : Dormancy in mammalian malaria. Trends Parasitol. 2012 ; 28 : 39-45.
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16 février 2012 4 16 /02 /février /2012 16:54

A novel lymphocyte transformation test (LTT-MELISA) for Lyme borreliosis.

Valentine-Thon E, Ilsemann K, Sandkamp M.

 

 

Department of Immunology, Laboratory Center Bremen, 28205 Bremen, Germany. evt@lanisa.de

 

 

Diagnosis of active Lyme borreliosis (LB) remains a challenge in clinically ambiguous, serologically indeterminant, and polymerase chain reaction-negative patients. 

Lymphocyte transformation tests (LTTs) have been applied to detect specific cellular immune reactivity, but their clinical application has been severely hampered by the poorly defined Borrelia antigens and nonstandardized LTT formats used. 

In this study, we describe the development and clinical relevance of a novel LTT using a validated format (MELISA) together with well-defined recombinant Borrelia-specific antigens. 

From an initial screening of 244 patients with suspected Borrelia infection or disease, 4 informative recombinant antigens were selected: OspC (Borrelia afzelii), p41-1 (Borrelia garinii), p41-2 (B. afzelii), and p100 (B. afzelii). 

Thereafter, 30 seronegative healthy controls were tested in LTT-MELISA(R) to determine specificity, 68 patients were tested in parallel to determine reproducibility, and 54 lymphocyte-reactive symptomatic patients were tested before and after antibiotic therapy to assess clinical relevance. 

Most (86.2%) of the 36.9% (90/244) LTT-MELISA positive patients were seropositive and showed symptoms of active LB. 

Specificity was 96.7% and reproducibility 92.6%. 

After therapy, most patients (90.7%) showed negative or markedly reduced lymphocyte reactivity correlating with clinical improvement. 

This novel LTT-MELISA assay appears to correlate with active LB and may have diagnostic relevance in confirming LB in clinically and serologically ambiguous cases.

 

Diagn Microbiol Infect Dis. 2007 Jan;57(1):27-34. Epub 2006 Jul 28.

 

PMID: 16876371 [PubMed - indexed for MEDLINE]

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12 février 2012 7 12 /02 /février /2012 21:21
Helminth parasites and the modulation of joint inflammation.

AuthorsMatisz CE, et al. Show all Journal
J Parasitol Res. 2011;2011:942616. Epub 2011 Apr 18.

Affiliation
Gastrointestinal Research Group, Department of Physiology and Pharmacology, The Calvin, Phoebe and Joan Snyder Institute of Infection Immunity and Inflammation, 1877 HSC University of Calgary, 3330 Hospital Drive NW, Calgary, AB, Canada T2N 4N1.

Abstract
There is an urgent need to develop better therapeutics for autoimmune and autoinflammatory diseases, of which musculoskeletal disorders such as rheumatoid arthritis are particularly prevalent and debilitating. Helminth parasites are accomplished masters at modifying their hosts' immune activity, and so attention has focused on rodent-helminth model systems to uncover the workings of the mammalian immune response to metazoan parasites, with the hope of revealing molecules and/or mechanisms that can be translated into better treatments for human autoimmune and idiopathic disorders. Substantial proof-of-principal data supporting the concept that infection with helminth parasites can reduce the severity of concomitant disease has been amassed from models of mucosal inflammation. Indeed, infection with helminth parasites has been tried as a therapy in inflammatory bowel disease, and there are case reports relating to other conditions (e.g., autism); however, the impact of infection with parasitic helminths on musculoskeletal diseases has not been extensively studied. Here, we present the view that such a strategy should be applied to the amelioration of joint inflammation and review the literature that supports this contention.
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12 février 2012 7 12 /02 /février /2012 21:14
Application of Novel PCR-Based Methods for Detection, Quantitation, and Phylogenetic Characterization of Sutterella Species in Intestinal Biopsy Samples from Children with Autism and Gastrointestinal Disturbances.

AuthorsWilliams BL, et al. Show all Journal
MBio. 2012 Jan 10;3(1). pii: e00261-11. doi: 10.1128/mBio.00261-11. Print 2012.

Affiliation
Center for Infection and Immunity, Mailman School of Public Health, Columbia University, New York, New York, USA.

Abstract
ABSTRACT Gastrointestinal disturbances are commonly reported in children with autism and may be associated with compositional changes in intestinal bacteria. In a previous report, we surveyed intestinal microbiota in ileal and cecal biopsy samples from children with autism and gastrointestinal dysfunction (AUT-GI) and children with only gastrointestinal dysfunction (Control-GI). Our results demonstrated the presence of members of the family Alcaligenaceae in some AUT-GI children, while no Control-GI children had Alcaligenaceae sequences. Here we demonstrate that increased levels of Alcaligenaceae in intestinal biopsy samples from AUT-GI children result from the presence of high levels of members of the genus Sutterella. We also report the first Sutterella-specific PCR assays for detecting, quantitating, and genotyping Sutterella species in biological and environmental samples. Sutterella 16S rRNA gene sequences were found in 12 of 23 AUT-GI children but in none of 9 Control-GI children. Phylogenetic analysis revealed a predominance of either Sutterella wadsworthensis or Sutterella stercoricanis in 11 of the individual Sutterella-positive AUT-GI patients; in one AUT-GI patient, Sutterella sequences were obtained that could not be given a species-level classification based on the 16S rRNA gene sequences of known Sutterella isolates. Western immunoblots revealed plasma IgG or IgM antibody reactivity to Sutterella wadsworthensis antigens in 11 AUT-GI patients, 8 of whom were also PCR positive, indicating the presence of an immune response to Sutterella in some children. IMPORTANCE Autism spectrum disorders affect ~1% of the population. Many children with autism have gastrointestinal (GI) disturbances that can complicate clinical management and contribute to behavioral problems. Understanding the molecular and microbial underpinnings of these GI issues is of paramount importance for elucidating pathogenesis, rendering diagnosis, and administering informed treatment. Here we describe an association between high levels of intestinal, mucoepithelial-associated Sutterella species and GI disturbances in children with autism. These findings elevate this little-recognized bacterium to the forefront by demonstrating that Sutterella is a major component of the microbiota in over half of children with autism and gastrointestinal dysfunction (AUT-GI) and is absent in children with only gastrointestinal dysfunction (Control-GI) evaluated in this study. Furthermore, these findings bring into question the role Sutterella plays in the human microbiota in health and disease. With the Sutterella-specific molecular assays described here, some of these questions can begin to be addressed.
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12 février 2012 7 12 /02 /février /2012 21:07
State of the art; microbiology in health and disease. Intestinal bacterial flora in autism.

Authors
Finegold SM.
Journal
Anaerobe. 2011 Dec;17(6):367-8. Epub 2011 Apr 16.

Affiliation
Veterans Administration Medical Center, Infectious Diseases Section (111F), Los Angeles, CA 90073, USA. sidfinegol@aol.com

Abstract
Autism of the regressive variety is selected as an example of the importance of intestinal bacterial microflora in disease other than classical infection.

Our studies have indicated that intestinal bacteria play a role in this disease since it responds to oral vancomycin, a drug that is not absorbed from the GI tract.

Pyrosequencing studies document an abnormal gut microflora in regressive autism subjects as compared to controls.

Finally, we present preliminary evidence suggesting that Desulfovibrio may play a key role in this disease.
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12 février 2012 7 12 /02 /février /2012 21:04
Maternal infection and immune involvement in autism.

Authors
Patterson PH.
Journal
Trends Mol Med. 2011 Jul;17(7):389-94. Epub 2011 Apr 7.

Affiliation
Biology Division, California Institute of Technology, Pasadena, CA 91125, USA. php@caltech.edu

Abstract
Recent studies have highlighted a connection between infection during pregnancy and the increased risk of autism in the offspring. Parallel studies of cerebral spinal fluid, blood and postmortem brains reveal an ongoing, hyper-responsive inflammatory-like state in many young as well as adult autism subjects.

There are also indications of gastrointestinal problems in at least a subset of autistic children. Work on the maternal infection risk factor using animal models indicates that aspects of brain and peripheral immune dysregulation can begin during fetal development and continue through adulthood.

The offspring of infected or immune-activated dams also display cardinal behavioral features of autism, as well as neuropathology consistent with that seen in human autism.

These rodent models are proving useful for the study of pathogenesis and gene-environment interactions as well as for the exploration of potential therapeutic strategies.
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