Maladie de Lyme

La maladie de Lyme est une maladie vectorielle et une zoonose (maladie infectieuse touchant l'être humain et de nombreux animaux). La maladie de Lyme est nommée d'après les villes de Lyme et Old Lyme, deux villes des États-Unis, dans l'État du Connecticut où elle a été signalée pour la première fois en 1975 et identifiée en 1977. Transmise par piqûre de tiques dures du genre Ixodes, c'est une maladie bactérienne, due à une borrélie (Borrelia burgdorferi, au sens étroit, prédominante en Amérique du Nord). L'expression borréliose de Lyme désigne souvent la « maladie de Lyme européenne », due à une plus grande diversité de borrélies (principalement Borrelia garinii, B. afzelii... ou B. burgdorferi au sens large). Maladie de Lyme et borréliose de Lyme sont souvent synonymes, dues alors à Borrelia burgdorferi au sens large. Les autres borrélioses sont dites fièvres récurrentes (cosmopolite transmise par poux, et régionales par tiques molles). La maladie se manifeste initialement par une éruption cutanée (érythème migrant) centrée sur une piqûre de tique. Non traitée, elle peut évoluer en trois stades de longue durée, caractérisés par une grande diversité car pouvant toucher plusieurs systèmes et organes. Elle se présente alors sous des formes plutôt cutanées, articulaires ou neurologiques, de façon aigüe ou chronique. La maladie est en expansion, devenue la plus fréquente des maladies vectorielles transmises à l'humain dans l'hémisphère nord. Dans près de 90 % des cas, elle est traitée efficacement par une antibiothérapie de . L'existence et la signification de formes non guéries par le traitement standard, ou l'attribution de pathologies chroniques à la maladie de Lyme, posent le problème de la « maladie chronique de Lyme ». La complexité du diagnostic clinique, l'interprétation problématique des tests sérologiques, des lignes directrices contestées pour le diagnostic, le traitement et la gestion antibiotique de la maladie de Lyme chronique entretiennent une controverse sociétale dite Lyme War aux États-Unis ou Scandale de Lyme en France.

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Mitochondrial respiratory chain dysfunction disrupts intracellular cholesterol homeostasis

Christopher Tadhg James Wall

Mitochondrial diseases are rare and severe conditions with debilitating symptoms. Biochemical defects in mitochondria however are common. The difference between these two frequencies is suspected to lie in the capability of the cells to adapt to the homeostatic disbalance. Cells activate retrograde signalling pathways in response to mitochondrial dysfunction, activating cellular transcriptional programs to correct for the disbalance. The full extent of the retrograde signals that are induced by mitochondrial dysfunctions still remains unknown. Studying these retrograde signalling pathways can lead to insights how to make the difference between restoring the homeostasis and a detrimental disease. Investigating the transcriptional responses to artificially induced mitochondrial dysfunction has proven to be lucrative in unveiling novel responses to mitochondrial defects. In this work we studied the transcriptional responses to three chemical models of mitochondrial respiratory chain dysfunction. In line with recently published work, we found a commonly upregulated stress response in all models. Interestingly, shared between all the models was a downregulation of genes enriched in cholesterol biosynthesis pathways. Upon closer examination this encompassed, almost without exception, all transcripts of the mevalonate pathway. This coordinated downregulation of transcripts had functional consequences on the output of the pathway, lowering the abundance of cholesterol precursor metabolites. Other metabolites in more upstream regions of the pathway were changed differently depending on the complex affected, suggesting other regulatory influences involved. Upon closer mechanistic investigation to the cause of the transcriptional suppression we found the main transcription factor responsible for mevalonate pathway gene transcription, the Sterol Response Element Binding Protein 2 (SREBP2), to be inhibited during complex I impairment. This was most evident in sterol depleted conditions where SREBP2 did not activate to normal levels. A decreased activation of SREBP2 is signature for an elevated concentration of ER-cholesterol. Indeed, other ER-bound cholesterol sensitive proteins confirmed this, showing a similar decreased abundance following complex I impairment in both normal and low lipid conditions. To investigate the source of this cholesterol we measured various cholesterol levels. No changes in the levels of total cholesterol (free cholesterol plus esterified cholesterol) were detected. Also, the fraction of free cholesterol was not significantly affected by complex I inhibition. Using the fluorescent cholesterol stain filipin, we were able to measure a modest but reproducible increase in intracellular free cholesterol. This provided novel mechanistic insight into the inhibition of ER sterol sensors and mevalonate pathway activity by mitochondrial dysfunction. Several well-known retrograde signalling pathways AMPK, ISR and mTOR did not explain the changes observed. The exact mechanism through which mitochondria incite an increase in intracellular free cholesterol remains unknown. Taken together this work can provide a mechanistic link between mitochondrial function and intracellular cholesterol homeostasis and could possibly link mitochondrial function to circulating lipoprotein homeostasis. Further work should focus on elucidating the possible mechanism, where differences in complex functions could provide a hint in the right direction.

EPFL2022

The human telomeric proteome during telomere replication

Joachim Lingner, Thomas Frédéric Lunardi, Aleksandra Vancevska, Gérald Joseph Paul Lossaint, Chih-Yi Gabriela Lin

Telomere shortening can cause detrimental diseases and contribute to aging. It occurs due to the end replication problem in cells lacking telomerase. Furthermore, recent studies revealed that telomere shortening can be attributed to difficulties of the semi-conservative DNA replication machinery to replicate the bulk of telomeric DNA repeats. To investigate telomere replication in a comprehensive manner, we develop QTIP-iPOND - Quantitative Telomeric chromatin Isolation Protocol followed by isolation of Proteins On Nascent DNA - which enables purification of proteins that associate with telomeres specifically during replication. In addition to the core replisome, we identify a large number of proteins that specifically associate with telomere replication forks. Depletion of several of these proteins induces telomere fragility validating their importance for telomere replication. We also find that at telomere replication forks the single strand telomere binding protein POT1 is depleted, whereas histone H1 is enriched. Our work reveals the dynamic changes of the telomeric proteome during replication, providing a valuable resource of telomere replication proteins. To our knowledge, this is the first study that examines the replisome at a specific region of the genome.

OXFORD UNIV PRESS2021

Maladie de Lyme

Borrelia burgdorferi

L'expression Borrelia burgdorferi peut désigner deux taxons ou entités bactériennes différentes de type Borrelia. Elle a été nommée ainsi en l'honneur de son découvreur, Willy Burgdorfer, qui l'a rendue responsable de la maladie de Lyme. Une bactérie pathogène (spirochète responsable d'une des formes, plutôt nord-américaine) de la maladie de Lyme. On parle alors de Borrelia burgdorferi ss ou stricto sensu (ss signifiant ici sensu stricto).

Viral meningitis

Viral meningitis, also known as aseptic meningitis, is a type of meningitis due to a viral infection. It results in inflammation of the meninges (the membranes covering the brain and spinal cord). Symptoms commonly include headache, fever, sensitivity to light and neck stiffness. Viruses are the most common cause of aseptic meningitis. Most cases of viral meningitis are caused by enteroviruses (common stomach viruses).

BIO-321: Morphology II

Ce cours permet aux étudiants ayant suivi Morphologie I de réviser et d'approfondir leurs connaissances par l'étude de l'anatomie radiologique et du développement. L'origine de malformations fréquente

CH-317: Drug discovery and development

This course discusses the molecular basis of diseases and how drugs work. Concepts and processes employed in today's drug discovery and development are covered. The first part of the course focuses on

BIO-480: Neuroscience: from molecular mechanisms to disease

The goal of the course is to guide students through the essential aspects of molecular neuroscience and neurodegenerative diseases. The student will gain the ability to dissect the molecular basis of

Explore les bases et le développement précoce des anticorps, y compris leur structure, fonction, diversité et application dans les maladies.

Couvre les variables thématiques dérivées des modèles numériques d'élévation pour l'analyse géospatiale.