Les pathologies cardio-vasculaires (CVD) representent la principale cause de morbidite et demortalite dans le monde. Le risque de CVD augmente avec l’âge, le tabagisme, le diabete, les dyslipidemies, l’obesite et l’insuffisance renale. L’incidence et la prevalence des CVD necessitent le developpement de strategies de prevention et de traitement, et la recherche de nouveaux biomarqueurs. Le recepteur aux produits de glycation avancee (RAGE) est implique dans plusieurs pathologies metaboliques ou inflammatoires. L’activation du RAGE par ses multiples ligands, i.e. produits de glycation avancee (AGE), proteines de la famille S100 et amphoterine (HMGB1) induit une cascade pro-inflammatoire. La forme soluble du RAGE (sRAGE) a ete proposee comme biomarqueur du risque vasculaire, de la severite et du devenir des CVD, particulierement chez les patients diabetiques ou insuffisants renaux. Cependant, les donnees sont contradictoires et des correlations positives et negatives sont observees pour une meme pathologie. L’importance de l’axe ligand-RAGE dans les processus pathologiques et le large eventail de molecules se liant au RAGE (des proteines proinflammatoires aux auto-anticorps), justifient le present travail. Au cours du present travail, dans un premier temps, nous avons d’abord etudie les effets des ligands du RAGE et des auto-anticorps anti-sRAGE recemment decrit, sur la quantification du sRAGE en ELISA. Nous supposons que l’interaction entre le sRAGE et ces molecules pourrait perturber le dosage du sRAGE. Dans un deuxieme travail, nous avons evalue les variations du taux de sRAGE et des auto-anticorps anti-sRAGE apres chirurgie bariatrique d’une obesite morbide. Les ligands du RAGE (Ne-carboxymethyllysine, S100A6, S100A12, S100B, HMGB1 et peptide β-amyloide) se fixent au sRAGE en differents sites et pourraient potentiellement interferer dans sa quantification par l’intermediaire d’un masquage d’epitope. Nous avons incube ces ligands, a des concentrations physiologiques et pathologiques, avec du sRAGE recombinant et du serum pour evaluer leur effet sur le dosage du sRAGE. Des auto-anticorps anti-sRAGE ont ete identifies et purifies et leur effet sur le dosage de sRAGE a ete evalue. La presence des ligands ou d’autoanticorps anti-sRAGE ne modifie pas le dosage du sRAGE recombinant ou serique. L’obesite favorise les dyslipidemies, les perturbations glycemiques et l’inflammation, conditions au cours desquelles le RAGE pourrait jouer un role important. Nous avons etudie les variations des taux seriques du sRAGE et de ses auto-anticorps et leur evolution avec l’amelioration metabolique des sujets obeses apres chirurgie bariatrique. Les patients ont ete selectionnes au sein d’une cohorte deja etablie (Patient presentant une obesite morbide et candidat a une chirurgie de bypass gastrique, ABOS, Lille). Les patients presentant des facteurs pouvant modifier les niveaux de sRAGE, tels qu’un traitement par statines, une insuffisance renale chronique ou une hypertension,ont ete exclus. Compare au groupe controle, les taux de sRAGE et d’auto-anticorps etaientsignificativement plus eleves chez les patients obeses avant la chirurgie. Parallelement a la baisse de l’indice de masse corporelle, les taux de sRAGE et d’anti-sRAGE ont ete significativement diminues un an apres la chirurgie. La baisse d’anti-sRAGE a ete correlee a l’augmentation des taux de HDL. Nous demontrons que les variations des taux de sRAGE constatees dans la litterature ne sont, a priori, pas dues a l’interaction des ligands du RAGE avec le sRAGE. D’autres hypotheses, comme la regulation de la formation et de la clairance du sRAGE, sont discutees. Nous avons, pour la premiere fois, demontre la presence d’auto-anticorps anti-sRAGE chez les patients obeses, et la diminution du taux de ces auto-anticorps apres une chirurgie de bariatrique. Ces resultats suggerent que l’obesite pourrait etre responsable d’une reaction auto-immune contre le sRAGE.

/pdf/value-of-rage-as-a-circulating-biomarker-from-srage-to-anti-1iganeu5yh.pdf

Value of RAGE as a circulating biomarker : from sRAGE to anti-sRAGE autoantibodies

We aimed to analyze markers of immune activation, inflammation, and oxidative stress in 92 asymptomatic HIV-infected patients according to the adequate (AR, >500 cells/mm3) or inadequate (IR,  nAR > LTNP > tAR > tIR. Higher levels of 8-isoprostane were observed in nIR. LTNP presented a higher retinol dosage than tAR and less genotoxic damage induced by oxidative stress than the other groups. We suggest that the therapy, despite being related to lesser immune activation and inflammation, alters the vitamin profile and consequently increases the oxidative stress of patients. In addition, the lowest genotoxic index for LTNP indicates that both VL and cART could be responsible for the increased DNA damage. More studies are needed to understand the influence of cART on persistent immune activation and inflammation.

/pdf/asymptomatic-hiv-people-present-different-profiles-of-scd14-5gh6wfetje.pdf

Asymptomatic HIV People Present Different Profiles of sCD14, sRAGE, DNA Damage, and Vitamins, according to the Use of cART and CD4+ T Cell Restoration.

Identification of biomarkers and/or mediators of cardiovascular disease (CVD) associated with HIV infection would be of diagnostic and therapeutic value. As soluble receptor for advanced glycation endproducts (sRAGE) and endogenous secretory (esRAGE) have been implicated in vascular complications in other settings, we investigated whether either soluble form of RAGE was associated with changes in carotid intima-media thickness (CIMT) in HIV-infected patients and HIV-uninfected controls. We found no differences in sRAGE, esRAGE, or CIMT among groups at study entry, or in yearly rates of change in sRAGE, esRAGE, or CIMT by HIV-serostatus (all p > 0.10). However, yearly rates of change in sRAGE (p = 0.07) and esRAGE (p < 0.001) were higher in those taking protease inhibitors, and lower baseline esRAGE levels (p = 0.06) were associated with increased odds of CIMT progression in HIV-infected individuals. Although esRAGE was not altered by HIV-serostatus (p = 0.17), its inverse relationship with CIMT progression in HIV-infected patients suggests a possible role as a mediator of CVD in HIV-infected persons.

Soluble Levels of Receptor for Advanced Glycation Endproducts (RAGE) and Progression of Atherosclerosis in Individuals Infected with Human Immunodeficiency Virus: ACTG NWCS 332

Low plasma levels of the soluble receptor for advanced glycation end products in HIV-infected patients with subclinical carotid atherosclerosis receiving combined antiretroviral therapy

https://ir.ymlib.yonsei.ac.kr/bitstream/22282913/93320/1/T201101521.pdf

쯔쯔가무시병 후에 발생한 anca 연관 혈관염에 의한 말초성 신경 염 1예

https://ir.ymlib.yonsei.ac.kr/bitstream/22282913/90403/1/T201204069.pdf

단백분해효소 억제제를 포함한 항레트로바이러스 병용 치료중인 HIV 감염 한국인에서 Atazanavir로 변경 후 지질 수치의 변화

골수염으로 발현된 재발성 콕시디오이데스 진균증 1예

https://ir.ymlib.yonsei.ac.kr/bitstream/22282913/93872/1/T201103074.pdf

카테터 집락화가 없는 지속성 캔디다혈증의 위험인자와 예후

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