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Relationship Between the ABO Blood Group and the Coronavirus Disease 2019 (COVID-19) Susceptibility.Clinical Infectious Diseases : An... Jul 2021To explore any relationship between the ABO blood group and the coronavirus disease 2019 (COVID-19) susceptibility, we compared ABO blood group distributions in 2173...
To explore any relationship between the ABO blood group and the coronavirus disease 2019 (COVID-19) susceptibility, we compared ABO blood group distributions in 2173 COVID-19 patients with local control populations, and found that blood group A was associated with an increased risk of infection, whereas group O was associated with a decreased risk.
Topics: ABO Blood-Group System; COVID-19; Disease Susceptibility; Humans; Retrospective Studies; SARS-CoV-2
PubMed: 32750119
DOI: 10.1093/cid/ciaa1150 -
Gut Microbes 2021The interaction disorder between gut microbiota and its host has been documented in different non-communicable diseases (NCDs) such as metabolic syndrome,... (Review)
Review
The interaction disorder between gut microbiota and its host has been documented in different non-communicable diseases (NCDs) such as metabolic syndrome, neurodegenerative disease, and autoimmune disease. The majority of these altered interactions arise through metabolic cross-talk between gut microbiota and host immune system, inducing a low-grade chronic inflammation that characterizes all NCDs. In this review, we discuss the contribution of bacterial metabolites to immune signaling pathways involved in NCDs. We then review recent advances that aid to rationally design microbial therapeutics. A deeper understanding of these intersections between host and gut microbiota metabolism using metabolomics-based system biology platform promises to reveal the fundamental mechanisms that drive metabolic predispositions to disease and suggest new avenues to use microbial therapeutic opportunities for NCDs treatment and prevention. : NCDs: non-communicable disease, IBD: inflammatory bowel disease, IL: interleukin, T2D: type 2 diabetes, SCFAs: short-chain fatty acids, HDAC: histone deacetylases, GPCR: G-protein coupled receptors, 5-HT: 5-hydroxytryptamine receptor signaling, DCs: dendritic cells, IECs: intestinal epithelial cells, T-reg: T regulatory cell, NF-κB: nuclear factor κB, TNF-α: tumor necrosis factor alpha, Th: T helper cell, CNS: central nervous system, ECs: enterochromaffin cells, NSAIDs: non-steroidal anti-inflammatory drugs, AhR: aryl hydrocarbon receptor, IDO: indoleamine 2,3-dioxygenase, QUIN: quinolinic acid, PC: phosphatidylcholine, TMA: trimethylamine, TMAO: trimethylamine -oxide, CVD: cardiovascular disease, NASH: nonalcoholic steatohepatitis, BAs: bile acids, FXR: farnesoid X receptor, CDCA: chenodeoxycholic acid, DCA: deoxycholic acid, LCA: lithocholic acid, UDCA: ursodeoxycholic acid, CB: cannabinoid receptor, COBRA: constraint-based reconstruction and analysis.
Topics: Amides; Bacteria; Bile Acids and Salts; Choline; Disease Susceptibility; Fatty Acids, Volatile; Gastrointestinal Microbiome; Humans; Immune System; Indoles; Noncommunicable Diseases; Polyamines; Signal Transduction; Vitamins
PubMed: 33590776
DOI: 10.1080/19490976.2021.1882927 -
Human Molecular Genetics Oct 2021Huntington's disease (HD) is a devastating neurogenetic disorder whose familial nature and progressive course were first described in the 19th century but for which no... (Review)
Review
Huntington's disease (HD) is a devastating neurogenetic disorder whose familial nature and progressive course were first described in the 19th century but for which no disease-modifying treatment is yet available. Through the active participation of HD families, this disorder has acted as a flagship for the application of human molecular genetic strategies to identify disease genes, understand pathogenesis and identify rational targets for development of therapies.
Topics: Alleles; Animals; Biomarkers; Disease Management; Disease Susceptibility; Genetic Association Studies; Genetic Linkage; Genetic Predisposition to Disease; Humans; Huntington Disease; Models, Biological
PubMed: 34169318
DOI: 10.1093/hmg/ddab170 -
Communications Biology Nov 2021Modern societies are experiencing an increasing trend of reduced sleep duration, with nocturnal sleeping time below the recommended ranges for health. Epidemiological... (Review)
Review
Modern societies are experiencing an increasing trend of reduced sleep duration, with nocturnal sleeping time below the recommended ranges for health. Epidemiological and laboratory studies have demonstrated detrimental effects of sleep deprivation on health. Sleep exerts an immune-supportive function, promoting host defense against infection and inflammatory insults. Sleep deprivation has been associated with alterations of innate and adaptive immune parameters, leading to a chronic inflammatory state and an increased risk for infectious/inflammatory pathologies, including cardiometabolic, neoplastic, autoimmune and neurodegenerative diseases. Here, we review recent advancements on the immune responses to sleep deprivation as evidenced by experimental and epidemiological studies, the pathophysiology, and the role for the sleep deprivation-induced immune changes in increasing the risk for chronic diseases. Gaps in knowledge and methodological pitfalls still remain. Further understanding of the causal relationship between sleep deprivation and immune deregulation would help to identify individuals at risk for disease and to prevent adverse health outcomes.
Topics: Disease Susceptibility; Humans; Immunity; Inflammation; Sleep Deprivation
PubMed: 34795404
DOI: 10.1038/s42003-021-02825-4 -
Minerva Medica Feb 2022
Topics: Asthma; Disease Susceptibility; Humans
PubMed: 34913639
DOI: 10.23736/S0026-4806.21.07958-1 -
Nature Immunology Jun 2020Impressive progress has been made over the last several years toward understanding how almost every aspect of the immune system contributes to the expression of systemic... (Review)
Review
Impressive progress has been made over the last several years toward understanding how almost every aspect of the immune system contributes to the expression of systemic autoimmunity. In parallel, studies have shed light on the mechanisms that contribute to organ inflammation and damage. New approaches that address the complicated interaction between genetic variants, epigenetic processes, sex and the environment promise to enlighten the multitude of pathways that lead to what is clinically defined as systemic lupus erythematosus. It is expected that each patient owns a unique 'interactome', which will dictate specific treatment.
Topics: Animals; Autoimmunity; Diagnosis, Differential; Disease Susceptibility; Environmental Exposure; Genetic Predisposition to Disease; Genetic Variation; Humans; Immunity, Innate; Lupus Erythematosus, Systemic; Lymphocyte Subsets; Organ Specificity; Sex Factors
PubMed: 32367037
DOI: 10.1038/s41590-020-0677-6 -
Journal of Clinical Immunology Oct 2019Regulatory T (Treg) cells expressing the transcription factor forkhead box P3 (Foxp3) play a requisite role in the maintenance of immunological homeostasis and... (Review)
Review
Regulatory T (Treg) cells expressing the transcription factor forkhead box P3 (Foxp3) play a requisite role in the maintenance of immunological homeostasis and prevention of peripheral self-tolerance breakdown. Although Foxp3 by itself is neither necessary nor sufficient to specify many aspects of the Treg cell phenotype, its sustained expression in Treg cells is indispensable for their phenotypic stability, metabolic fitness, and regulatory function. In this review, we summarize recent advances in Treg cell biology, with a particular emphasis on the role of Foxp3 as a transcriptional modulator and metabolic gatekeeper essential to an effective immune regulatory response. We discuss these findings in the context of human inborn errors of immune dysregulation, with a focus on FOXP3 mutations, leading to Treg cell deficiency. We also highlight emerging concepts of therapeutic Treg cell reprogramming to restore tolerance in the settings of immune dysregulatory disorders.
Topics: Animals; Biomarkers; Cell Communication; Cell Differentiation; Cellular Reprogramming; Disease Susceptibility; Energy Metabolism; Forkhead Transcription Factors; Gene Expression Regulation; Humans; Immune Tolerance; Immunomodulation; Immunotherapy; Organ Specificity; Phenotype; T-Lymphocyte Subsets; T-Lymphocytes, Regulatory
PubMed: 31478130
DOI: 10.1007/s10875-019-00684-7 -
Frontiers in Immunology 2021During an inflammatory process, shift in the cellular metabolism associated with an increase in extracellular acidification are well-known features. This pH drop in the... (Review)
Review
During an inflammatory process, shift in the cellular metabolism associated with an increase in extracellular acidification are well-known features. This pH drop in the inflamed tissue is largely attributed to the presence of lactate by an increase in glycolysis. In recent years, evidence has accumulated describing the role of lactate in inflammatory processes; however, there are differences as to whether lactate can currently be considered a pro- or anti-inflammatory mediator. Herein, we review these recent advances on the pleiotropic effects of lactate on the inflammatory process. Taken together, the evidence suggests that lactate could exert differential effects depending on the metabolic status, cell type in which the effects of lactate are studied, and the pathological process analyzed. Additionally, various targets, including post-translational modifications, G-protein coupled receptor and transcription factor activation such as NF-κB and HIF-1, allow lactate to modulate signaling pathways that control the expression of cytokines, chemokines, adhesion molecules, and several enzymes associated with immune response and metabolism. Altogether, this would explain its varied effects on inflammatory processes beyond its well-known role as a waste product of metabolism.
Topics: Animals; Biological Transport; Biomarkers; Cytokines; Disease Susceptibility; Energy Metabolism; Humans; Immunomodulation; Inflammation; Inflammation Mediators; Lactic Acid; Metabolic Networks and Pathways; Organ Specificity; Receptors, G-Protein-Coupled
PubMed: 35095895
DOI: 10.3389/fimmu.2021.808799 -
Neuropharmacology Mar 2021Addiction is a chronic brain disease that has dramatic health and socioeconomic consequences worldwide. Multiple approaches have been used for decades to clarify the... (Review)
Review
Addiction is a chronic brain disease that has dramatic health and socioeconomic consequences worldwide. Multiple approaches have been used for decades to clarify the neurobiological basis of this disease and to identify novel potential treatments. This review summarizes the main brain networks involved in the vulnerability to addiction and specific innovative technological approaches to investigate these neural circuits. First, the evolution of the definition of addiction across the Diagnostic and Statistical Manual of Mental Disorders (DSM) is revised. We next discuss several innovative experimental techniques that, combined with behavioral approaches, have allowed recent critical advances in understanding the neural circuits involved in addiction, including DREADDs, calcium imaging, and electrophysiology. All these techniques have been used to investigate specific neural circuits involved in vulnerability to addiction and have been extremely useful to clarify the neurobiological basis of each specific component of the addictive process. These novel tools targeting specific brain regions are of great interest to further understand the different aspects of this complex disease. This article is part of the special issue on 'Vulnerabilities to Substance Abuse.'.
Topics: Animals; Behavior, Addictive; Brain; Calcium Signaling; Disease Susceptibility; Electroencephalography; Electrophysiological Phenomena; Humans; Illicit Drugs; Nerve Net; Piperazines
PubMed: 33482225
DOI: 10.1016/j.neuropharm.2021.108466 -
British Journal of Haematology Jan 2022Paroxysmal nocturnal haemoglobinuria (PNH) is characterized by complement-mediated intravascular haemolysis, severe thrombophilia and bone marrow failure. While for... (Review)
Review
Paroxysmal nocturnal haemoglobinuria (PNH) is characterized by complement-mediated intravascular haemolysis, severe thrombophilia and bone marrow failure. While for patients with bone marrow failure the treatment follows that of immune-mediated aplastic anaemia, that of classic, haemolytic PNH is based on anti-complement medication. The anti-C5 monoclonal antibody eculizumab has revolutionized treatment, resulting in control of intravascular haemolysis and thromboembolic risk, with improved long-term survival. Novel strategies of complement inhibition are emerging. New anti-C5 agents reproduce the safety and efficacy of eculizumab, with improved patient convenience. Proximal complement inhibitors have been developed to address C3-mediated extra-vascular haemolysis and seem to improve haematological response.
Topics: Algorithms; Clinical Decision-Making; Combined Modality Therapy; Disease Management; Disease Susceptibility; Genetic Predisposition to Disease; Hemoglobinuria, Paroxysmal; Humans; Phenotype; Prognosis; Standard of Care; Treatment Outcome
PubMed: 34355382
DOI: 10.1111/bjh.17753