Database : MEDLINE
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[PMID]: 29510755
[Au] Autor:Calender A; Rollat Farnier PA; Buisson A; Pinson S; Bentaher A; Lebecque S; Corvol H; Abou Taam R; Houdouin V; Bardel C; Roy P; Devouassoux G; Cottin V; Seve P; Bernaudin JF; Lim CX; Weichhart T; Valeyre D; Pacheco Y; Clement A; Nathan N; in the frame of GSF (Groupe Sarcoïdose France)
[Ad] Address:Genetics Department, Hospices Civils de LYON (HCL), University Hospital, East Pathology Center, LYON, B-A3, 59 Bld Pinel, 69677, BRON Cedex, France. alain.calender@chu-lyon.fr.
[Ti] Title:Whole exome sequencing in three families segregating a pediatric case of sarcoidosis.
[So] Source:BMC Med Genomics;11(1):23, 2018 Mar 06.
[Is] ISSN:1755-8794
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: Sarcoidosis (OMIM 181000) is a multi-systemic granulomatous disorder of unknown origin. Despite multiple genome-wide association (GWAS) studies, no major pathogenic pathways have been identified to date. To find out relevant sarcoidosis predisposing genes, we searched for de novo and recessive mutations in 3 young probands with sarcoidosis and their healthy parents using a whole-exome sequencing (WES) methodology. METHODS: From the SARCFAM project based on a national network collecting familial cases of sarcoidosis, we selected three families (trios) in which a child, despite healthy parents, develop the disease before age 15 yr. Each trio was genotyped by WES (Illumina HiSEQ 2500) and we selected the gene variants segregating as 1) new mutations only occurring in affected children and 2) as recessive traits transmitted from each parents. The identified coding variants were compared between the three families. Allelic frequencies and in silico functional results were analyzed using ExAC, SIFT and Polyphenv2 databases. The clinical and genetic studies were registered by the ClinicalTrials.gov - Protocol Registration and Results System (PRS) ( https://clinicaltrials.gov ) receipt under the reference NCT02829853 and has been approved by the ethical committee (CPP LYON SUD EST - 2 - REF IRB 00009118 - September 21, 2016). RESULTS: We identified 37 genes sharing coding variants occurring either as recessive mutations in at least 2 trios or de novo mutations in one of the three affected children. The genes were classified according to their potential roles in immunity related pathways: 9 to autophagy and intracellular trafficking, 6 to G-proteins regulation, 4 to T-cell activation, 4 to cell cycle and immune synapse, 2 to innate immunity. Ten of the 37 genes were studied in a bibliographic way to evaluate the functional link with sarcoidosis. CONCLUSIONS: Whole exome analysis of case-parent trios is useful for the identification of genes predisposing to complex genetic diseases as sarcoidosis. Our data identified 37 genes that could be putatively linked to a pediatric form of sarcoidosis in three trios. Our in-depth focus on 10 of these 37 genes may suggest that the formation of the characteristic lesion in sarcoidosis, granuloma, results from combined deficits in autophagy and intracellular trafficking (ex: Sec16A, AP5B1 and RREB1), G-proteins regulation (ex: OBSCN, CTTND2 and DNAH11), T-cell activation (ex: IDO2, IGSF3), mitosis and/or immune synapse (ex: SPICE1 and KNL1). The significance of these findings needs to be confirmed by functional tests on selected gene variants.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[Cl] Clinical Trial:ClinicalTrial
[St] Status:In-Data-Review
[do] DOI:10.1186/s12920-018-0338-x

  2 / 71133 MEDLINE  
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[PMID]: 29505764
[Au] Autor:Asojo OA; Darwiche R; Gebremedhin S; Smant G; Lozano-Torres JL; Drurey C; Pollet J; Maizels RM; Schneiter R; Wilbers RHP
[Ad] Address:National School of Tropical Medicine, Baylor College of Medicine, Houston, TX 77030, USA. Electronic address: asojo@bcm.edu.
[Ti] Title:Heligmosomoides polygyrus Venom Allergen-like Protein-4 (HpVAL-4) is a sterol binding protein.
[So] Source:Int J Parasitol;, 2018 Mar 02.
[Is] ISSN:1879-0135
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Heligmosomoides polygyrus bakeri is a model parasitic hookworm used to study animal and human helminth diseases. During infection, the parasite releases excretory/secretory products that modulate the immune system of the host. The most abundant protein family in excretory/secretory products comprises the venom allergen-like proteins (VALs), which are members of the SCP/TAPS (sperm-coating protein/Tpx/antigen 5/pathogenesis related-1/Sc7) superfamily. There are >30 secreted Heligmosomoides polygyrus VAL proteins (HpVALs) and these proteins are characterised by having either one or two 15 kDa CAP (cysteine-rich secretory protein (CRISP)/antigen 5/pathogenesis related-1) domains. The first known HpVAL structure, HpVAL-4, refined to 1.9 Šis reported. HpVAL-4 was produced as a homogeneously glycosylated protein in leaves of Nicotiana benthamiana infiltrated with recombinant plasmids, making this plant expression platform amenable for the production of biological products. The overall topology of HpVAL-4 is a three layered αßα sandwich between a short N-terminal loop and a C-terminal cysteine rich extension. The C-terminal cysteine rich extension has two strands stabilized by two disulfide bonds and superposes well with the previously reported extension from the human hookworm Necator americanus Ancylostoma secreted protein-2 (Na-ASP-2). The N-terminal loop is connected to alpha helix 2 via a disulfide bond previously observed in Na-ASP-2. HpVAL-4 has a central cavity that is more similar to the N-terminal CAP domain of the two CAP Na-ASP-1 from Necator americanus. Unlike Na-ASP-2, mammalian CRISP, and the C-terminal CAP domain of Na-ASP-1, the large central cavity of HpVAL-4 lacks the two histidines required to coordinate divalent cations. HpVAL-4 has both palmitate-binding and sterol-binding cavities and is able to complement the in vivo sterol export phenotype of yeast mutants lacking their endogenous CAP proteins. More studies are required to determine endogenous binding partners of HpVAL-4 and unravel the possible impact of sterol binding on immune-modulatory functions.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  3 / 71133 MEDLINE  
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[PMID]: 29412048
[Au] Autor:Caldwell RW; Rodriguez PC; Toque HA; Narayanan SP; Caldwell RB
[Ad] Address:Department of Pharmacology & Toxicology, Vision Discovery Institute, Department of Medicine-Hematology and Oncology, Department of Occupational Therapy, School of Allied Health Sciences, and Vascular Biology Center, Medical College of Georgia, Augusta University , Augusta, Georgia ; and VA Medic
[Ti] Title:Arginase: A Multifaceted Enzyme Important in Health and Disease.
[So] Source:Physiol Rev;98(2):641-665, 2018 Apr 01.
[Is] ISSN:1522-1210
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The arginase enzyme developed in early life forms and was maintained during evolution. As the last step in the urea cycle, arginase cleaves l-arginine to form urea and l-ornithine. The urea cycle provides protection against excess ammonia, while l-ornithine is needed for cell proliferation, collagen formation, and other physiological functions. In mammals, increases in arginase activity have been linked to dysfunction and pathologies of the cardiovascular system, kidney, and central nervous system and also to dysfunction of the immune system and cancer. Two important aspects of the excessive activity of arginase may be involved in diseases. First, overly active arginase can reduce the supply of l-arginine needed for the production of nitric oxide (NO) by NO synthase. Second, too much l-ornithine can lead to structural problems in the vasculature, neuronal toxicity, and abnormal growth of tumor cells. Seminal studies have demonstrated that increased formation of reactive oxygen species and key inflammatory mediators promote this pathological elevation of arginase activity. Here, we review the involvement of arginase in diseases affecting the cardiovascular, renal, and central nervous system and cancer and discuss the value of therapies targeting the elevated activity of arginase.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review
[do] DOI:10.1152/physrev.00037.2016

  4 / 71133 MEDLINE  
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[PMID]: 29228214
[Au] Autor:Kim RY; Mangu D; Hoffman AS; Kavosh R; Jung E; Itoh N; Voskuhl R
[Ad] Address:Multiple Sclerosis Program, Department of Neurology, David Geffen School of Medicine, University of California, Los Angeles, CA 90095, USA.
[Ti] Title:Oestrogen receptor β ligand acts on CD11c+ cells to mediate protection in experimental autoimmune encephalomyelitis.
[So] Source:Brain;141(1):132-147, 2018 01 01.
[Is] ISSN:1460-2156
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Oestrogen treatments are neuroprotective in a variety of neurodegenerative disease models. Selective oestrogen receptor modifiers are needed to optimize beneficial effects while minimizing adverse effects to achieve neuroprotection in chronic diseases. Oestrogen receptor beta (ERβ) ligands are potential candidates. In the multiple sclerosis model chronic experimental autoimmune encephalomyelitis, ERβ-ligand treatment is neuroprotective, but mechanisms underlying this neuroprotection remain unclear. Specifically, whether there are direct effects of ERβ-ligand on CD11c+ microglia, myeloid dendritic cells or macrophages in vivo during disease is unknown. Here, we generated mice with ERβ deleted from CD11c+ cells to show direct effects of ERβ-ligand treatment in vivo on these cells to mediate neuroprotection during experimental autoimmune encephalomyelitis. Further, we use bone marrow chimeras to show that ERβ in peripherally derived myeloid cells, not resident microglia, are the CD11c+ cells mediating this protection. CD11c+ dendritic cell and macrophages isolated from the central nervous system of wild-type experimental autoimmune encephalomyelitis mice treated with ERβ-ligand expressed less iNOS and T-bet, but more IL-10, and this treatment effect was lost in mice with specific deletion of ERβ in CD11c+ cells. Also, we extend previous reports of ERβ-ligand’s ability to enhance remyelination through a direct effect on oligodendrocytes by showing that the immunomodulatory effect of ERβ-ligand acting on CD11c+ cells is necessary to permit the maturation of oligodendrocytes. Together these results demonstrate that targeting ERβ signalling pathways in CD11c+ myeloid cells is a novel strategy for regulation of the innate immune system in neurodegenerative diseases. To our knowledge, this is the first report showing how direct effects of a candidate neuroprotective treatment on two distinct cell lineages (bone marrow derived myeloid cells and oligodendrocytes) can have complementary neuroprotective effects in vivo.awx315media15688130498001.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review
[do] DOI:10.1093/brain/awx315

  5 / 71133 MEDLINE  
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[PMID]: 29524196
[Au] Autor:Tripathi D; Mani V; Pal RP
[Ad] Address:National Dairy Research Institute, Karnal, Haryana, India. deepika.trip03@gmail.com.
[Ti] Title:Vanadium in Biosphere and Its Role in Biological Processes.
[So] Source:Biol Trace Elem Res;, 2018 Mar 09.
[Is] ISSN:1559-0720
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Ultra-trace elements or occasionally beneficial elements (OBE) are the new categories of minerals including vanadium (V). The importance of V is attributed due to its multifaceted biological roles, i.e., glucose and lipid metabolism as an insulin-mimetic, antilipemic and a potent stress alleviating agent in diabetes when vanadium is administered at lower doses. It competes with iron for transferrin (binding site for transportation) and with lactoferrin as it is secreted in milk also. The intracellular enzyme protein tyrosine phosphatase, causing the dephosphorylation at beta subunit of the insulin receptor, is inhibited by vanadium, thus facilitating the uptake of glucose inside the cell but only in the presence of insulin. Vanadium could be useful as a potential immune-stimulating agent and also as an antiinflammatory therapeutic metallodrug targeting various diseases. Physiological state and dose of vanadium compounds hold importance in causing toxicity also. Research has been carried out mostly on laboratory animals but evidence for vanadium importance as a therapeutic agent are available in humans and large animals also. This review examines the potential biochemical and molecular role, possible kinetics and distribution, essentiality, immunity, and toxicity-related study of vanadium in a biological system.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher
[do] DOI:10.1007/s12011-018-1289-y

  6 / 71133 MEDLINE  
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[PMID]: 29523289
[Au] Autor:Diani SDS
[Ad] Address:Independent Researcher, Mantova, Italy. Electronic address: dr.saradiani@gmail.com.
[Ti] Title:A new model for chronic diseases.
[So] Source:Med Hypotheses;113:30-39, 2018 Apr.
[Is] ISSN:1532-2777
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Chronic diseases are defined diseases whose symptoms last for at least six months and tend to worsen over time. In Europe, they cause at least 86% of deaths. In this speculative unifying model I set a new hypothesis for the etiology of the majority of chronic diseases. The main aim is to put order and observe our organism in a systemic way, connecting pathologies we now see as disconnected phenomena, with the conceptual frameworks of complex systems and network medicine. Chronic diseases could be caused by a first unsolved acute infection. In case the pathogen cannot be completely eliminated, it becomes a persistent infectious. After the acute episode, some mild symptoms will occur and probably disappear; the chronic disease will remain latent over time. It will manifest even after years or decades, in the presence of another acute infection, a particular stress, trauma, or another event. The presence of the persistent infectious elicits changes in the immune and systemic regulation, and these processes degenerate over time. They will assume their rules and patterns, being independent from the initial stimulus. The key to understand the dynamics and individuality of chronic diseases is the immune system and its networks. The immune mechanisms that can lead to the persistent response are mainly the switch from the Th1 to the Th2 immunity and the molecular mimicry. The first persistent infectious will also modify the susceptibility to other pathogens, facilitating new infections and new consequent persistent infectious. From the immune point of view, our organism is divided into three compartments: the outer one, which comprehend all the surfaces in contact with the environment, the intermediate one, which comprehend the internal organs and tissues, and the innermost one, comprehending the Central Nervous System and the adluminal compartment of the seminiferous tubule. The immune key-role is played respectively by the mucosa-associated lymphoid tissue, the endothelium, the blood-brain barrier and blood-testis barrier. The chronic diseases follow a progressive scheme, involving the three compartments from the outer to the innermost one. The primer microorganism at the origin of the majority of diseases could be streptococcus, or staphylococcus. Both cause acute in children, with a great variability of responses and symptoms, and both cause molecular mimicry. This model can be tested and proved in more ways, I propose here some of them. It could pave the way to a radical change in our comprehension and therapeutic approaches to chronic diseases.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:In-Process

  7 / 71133 MEDLINE  
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[PMID]: 29522800
[Au] Autor:Gahoi S; Singh S; Gautam B
[Ad] Address:Department of Computational Biology and Bioinformatics, Sam Higginbottom University of Agriculture, Technology and Sciences, Allahabad 211007, India. Electronic address: shachigahoimbi@gmail.com.
[Ti] Title:Genome-wide identification and comprehensive analysis of excretory/secretory proteins in nematodes provide potential drug targets for parasite control.
[So] Source:Genomics;, 2018 Mar 06.
[Is] ISSN:1089-8646
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Nematodes are responsible for causing severe diseases in plants, humans and other animals. Infection is associated with the release of excretory/secretory (ES) proteins into host cytoplasm and interference with the host immune system which make them attractive targets for therapeutic use. The identification of ES proteins through bioinformatics approaches is cost- and time-effective and could be used for screening of potential targets for parasitic diseases for further experimental studies. Here, we identified and functionally annotated 93,949 ES proteins, in the genome of 73 nematodes using integration of various bioinformatics tools. 30.6% of ES proteins were supported at RNA level. The predicted ES proteins, annotated by gene ontology terms, domains, pathways, proteases and enzyme class analysis were enriched in molecular functions of proteases, protease inhibitors, c-type lectin and hydrolases which are strongly associated with typical functions of ES proteins. We identified a total of 492 ES proteins from human and plant parasitic nematodes, homologues to DrugBank-approved targets and C. elegans RNA interference gene database which could represent potential targets for parasite control. This comprehensive analysis of nematode secretome provide valuable resource for further experimental studies to understand host-pathogen interactions and novel therapeutic solutions for parasitic infections.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher

  8 / 71133 MEDLINE  
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[PMID]: 29522782
[Au] Autor:Bassi GS; Ulloa L; Santos VR; Del Vecchio F; Delfino-Pereira P; Rodrigues GJ; Castania JA; Cunha FQ; Salgado HC; Cunha TM; Garcia-Cairasco N; Kanashiro A
[Ad] Address:Department of Immunology, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, SP, Brazil; Translational Research Center for GastroIntestinal Disorders (TARGID), Intestinal Neuroimmune Interactions, University of Leuven, Leuven, Belgium. Electronic address: shimizug@gmail.com.
[Ti] Title:Cortical stimulation in conscious rats controls joint inflammation.
[So] Source:Prog Neuropsychopharmacol Biol Psychiatry;, 2018 Mar 06.
[Is] ISSN:1878-4216
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:The neuronal control of the immune system is fundamental to the development of new therapeutic strategies for inflammatory disorders. Recent studies reported that afferent vagal stimulation attenuates peripheral inflammation by activating specific sympathetic central and peripheral networks, but only few subcortical brain areas were investigated. In the present study, we report that afferent vagal stimulation also activates specific cortical areas, as the parietal and cingulate cortex. Since these cortical structures innervate sympathetic-related areas, we investigate whether electrical stimulation of parietal cortex can attenuate knee joint inflammation in non-anesthetized rats. Our results show that cortical stimulation in rats increased sympathetic activity and improved joint inflammatory parameters, such as local neutrophil infiltration and pro-inflammatory cytokine levels, without causing behavioral disturbance, brain epileptiform activity or neural damage. In addition, we superposed the areas activated by afferent vagal or cortical stimulation to map common central structures to depict a brain immunological homunculus that can allow novel therapeutic approaches against inflammatory joint diseases, such as rheumatoid arthritis.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher

  9 / 71133 MEDLINE  
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[PMID]: 29522425
[Au] Autor:Ma Q; Yu Q; Xing X; Liu S; Shi C; Luo J
[Ad] Address:School of Traditional Chinese Medical Science, Southern Medical University, Guangzhou 510515, China. 13268268214@163.com.
[Ti] Title:San Wu Huangqin Decoction, a Chinese Herbal Formula, Inhibits Influenza a/PR/8/34 (H1N1) Virus Infection In Vitro and In Vivo.
[So] Source:Viruses;10(3), 2018 Mar 09.
[Is] ISSN:1999-4915
[Cp] Country of publication:Switzerland
[La] Language:eng
[Ab] Abstract:The San Wu Huangqin Decoction (SWHD), a traditional Chinese medicine formula, is used to treat colds caused by exposure to wind-pathogen, hyperpyrexia, infectious diseases and cancer; moreover, it is used for detoxification. The individual herbs of SWHD, such as and , exhibit a wide spectrum of antiviral, anti-inflammatory, antibacterial, anticancer and other properties. The Chinese compound formula of SWHD is composed of and . However, the effect of SWHD on the influenza virus (IFV) and its mechanism remain unknown. The aim of this study was to evaluate, for the first time, whether SWHD could be used to treat influenza. Results showed that SWHD could effectively inhibit influenza A/PR/8/34 (H1N1) virus at different stages of viral replication (confirmed through antiviral effect assay, penetration assay, attachment assay and internalization assay) in vitro. It could reduce the infection of the virus in a dose- and time-dependent manner, as confirmed by observing the cell cytopathic effect and calculating the cell viability ( < 0.05). SWHD demonstrated better antiviral activity than oseltamivir in the evaluation of antiviral prophylaxis on influenza ( < 0.05). The antiviral activity of SWHD may be related to its regulation ability on the immune system. Western blot, real-time polymerase chain reaction and indirect immunofluorescence assay showed that the expression of the four target viral proteins of the IFV (namely, haemagglutinin (HA), neuraminidase (NA), nucleoprotein (NP) and matrix-2 (M2)) reduced significantly ( < 0.05). Moreover, SWHD (23.40 and 11.70 g/kg) significantly alleviated the clinical signs, reduced the mortality and increased the survival time of infected mice ( < 0.05). The lung index, virus titres, pathological changes in lung tissues and the expression of key proteins of the IFV in mice also decreased ( < 0.05). In conclusion, SWHD possessed anti-influenza activity. This work provided a new view of complementary therapy and drug discovery for clinical treatment.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Data-Review

  10 / 71133 MEDLINE  
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[PMID]: 29506719
[Au] Autor:Geovanini GR; Wang R; Weng J; Tracy R; Jenny NS; Goldberger AL; Costa MD; Liu Y; Libby P; Redline S
[Ad] Address:Department of Medicine, Division of Sleep and Circadian Disorders, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. Electronic address: ggeovanini@hsph.harvard.edu.
[Ti] Title:Elevations in neutrophils with obstructive sleep apnea: The Multi-Ethnic Study of Atherosclerosis (MESA).
[So] Source:Int J Cardiol;257:318-323, 2018 Apr 15.
[Is] ISSN:1874-1754
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:BACKGROUND: Obstructive sleep apnea (OSA) associates with increased risk of cardiovascular diseases (CVD). Immune abnormalities and surges in sympathetic activity accompany OSA and CVD. We hypothesized that OSA associates with leukocytosis partially by abnormalities in autonomic nervous system (ANS) function that would suggest a pathway linking OSA and CVD. METHODS: Participants from the Multi-Ethnic Study of Atherosclerosis (MESA), a prospective cohort of individuals initially without overt CVD, underwent polysomnography and assays for white blood cells (WBC) and subsets. Heart rate (HR) and heart rate variability (HRV), indirect measurements of ANS, were obtained from overnight electrocardiography. A formal statistical mediation analysis tested the indirect effect that mean HR and HRV measures contribute to associations between OSA and leukocytosis. RESULTS: The analytical sample consisted of 1298 participants (54% female), ages 54-93years, 14% with severe OSA (apnea-hypopnea-index, AHI≥30). Severe OSA associated with a higher prevalence of obesity, diabetes, and increased levels of WBC total and subsets. Neutrophil count associated with severe OSA after adjusting for confounders (p=0.017). Mean HR positively associated with OSA indices and neutrophils. A mediation analysis revealed an "indirect" effect of mean HR that explained an estimated 11% of the association between AHI and neutrophils. Overnight hypoxia also associated with neutrophil count (p=0.009), and mean HR explained 14% of the association between neutrophils and hypoxia. CONCLUSIONS: In the MESA cohort, OSA measures associate with elevated neutrophil counts and increases in overnight mean HR. These data link innate immune dysregulation with OSA and provide a potential pathophysiologic pathway between CVD and OSA.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:In-Data-Review


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