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 previously reported the presence of memory CD4+ T cells that express low levels of SAMHD1 (SAMHD1low) in peripheral blood and lymph nodes from both HIV-1 infected and uninfected individuals. These cells are enriched in Th17 and Tfh subsets, two populations known to be preferentially targeted by HIV-1. Here we investigated whether SAMHD1low CD4+ T-cells harbour replication-competent virus and compartimentalized HIV-1 genomes. We sorted memory CD4+CD45RO+SAMHD1low, CD4+CD45RO+SAMHD1+ and naive CD4+CD45RO-SAMHD1+ cells from HIV-1-infected patients on anti-retroviral therapy (c-ART) and performed HIV-1 DNA quantification, ultra-deep-sequencing of partial env (C2/V3) sequences and phenotypic characterization of the cells. We show that SAMHD1low cells include novel Th17 CCR6+ subsets that lack CXCR3 and CCR4 (CCR6+DN). There is a decrease of the % of Th17 in SAMHD1low compartment in infected compared to uninfected individuals (41% vs 55%, p<0.05), whereas the % of CCR6+DN increases (7.95% vs 3.8%, p<0.05). Moreover, in HIV-1 infected patients, memory SAMHD1low cells harbour high levels of HIV-1 DNA compared to memory SAMHD1+ cells (4.5 vs 3.8 log/106cells, respectively, p<0.001), while naive SAMHD1+ showed significantly lower levels (3.1 log/106cells, p<0.0001). Importantly, we show that SAMHD1low cells contain p24-producing cells. Moreover, phylogenetic analyses revealed well-segregated HIV-1 DNA populations with compartmentalization between SAMHD1low and SAMHD1+ memory cells, and limited viral exchange. As expected, the % of Ki67+ cells was significantly higher in SAMHD1low compared to SAMHD1+ cells. There was positive association between levels of HIV-1 DNA and Ki67+ in memory SAMHD1low cells, but not in memory and naive SAMHD1+ CD4+ T-cells. Altogether, these data suggest that proliferative memory SAMHD1low cells contribute to viral persistence.

Proliferative memory SAMHD1low CD4+ T cells harbour high levels of HIV-1 with compartmentalized viral populations

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

HIV migration between blood plasma and cellular subsets before and after HIV therapy

https://ir.ymlib.yonsei.ac.kr/bitstream/22282913/86297/1/T201300267.pdf

지역사회에서 획득된 Acinetobacter baumannii에 의한 감염성 심내막염 1예

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

HIV migration between blood plasma and cellular subsets before and after HIV therapy

지역사회에서 획득된 Acinetobacter baumannii에 의한 감염성 심내막염 1예