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The innate immune system has evolved means to recognize and react suitably to foreign entities such as infectious agents. In many cases infectious microorganisms threaten the integrity and function of the target organs or tissues; therefore, consequent to their recognition the immune system becomes activated to ensure their elimination. Toll-like receptors (TLR) constitute a family of receptors specialized in the recognition of molecular patterns typically associated with infectious agents. Different TLRs exist, each selective for molecular entities and motifs belonging to a specific pathogen group. Consequently, it is thought that the molecular nature of invading microorganisms activates specific TLRs to drive adequate anti-infectious immunity. For instance, nucleic acid-specific, intracellular receptors (TLR3/7/8/9) are used to sense viruses and drive antiviral immunity, while other receptors (such as TLR2 and TLR4) recognize and promote immunity against bacteria, yeast, and fungi. Yet, it is becoming evident that activation of TLR pathways trigger mechanisms that not only stimulate but also regulate the immune system. For instance, TLR stimulation by viruses will drive antiviral interferon but also immunoregulatory cytokine production and regulatory T cell activation. Stimulation of TLRs by bacteria or using molecular agonists can also trigger both immune stimulatory and regulatory responses. TLR stimulation by infectious agents likely serves to activate but also control anti-infectious immunity, for instance prevent potential immunopathological tissue damage which can be caused by acute immune defense mechanisms. Previous work by us and others has shown that the immunoregulatory arm of TLR stimulation can additionally help control autoreactive processes in autoimmune disease. Hence, it is becoming established that gut commensals, which also play a crucial part in the control of autoimmune disease, establish immune regulatory mechanisms through activation of particular TLRs. In sum, it appears that TLRs are key immune players that not only stimulate but also regulate immune processes in health and disease. In this Research Topic, we wish to review the dual role of TLRs as activators and regulators of immune responses. We aim to motivate data-driven opinions as to the importance of context of TLR agonism for determining immune activation vs. regulation. The presentation of ongoing original works, as well as data and opinions around other innate immune receptors pertaining to this topic, are also encouraged.
Infection --- Toll-Like Receptors --- Probiotics --- Immune stimulation --- Immunoregulation --- Autoimmune Diseases --- cancer immunotherapy --- Inflammation --- microbiome --- tolerance
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The group of pattern recognition receptors (PRRs) includes families of Toll-like receptors (TLRs), NOD-like receptors (NLRs), C-type lectin receptors (CLRs), RIG-I-like receptors (RLRs), and AIM-2-like receptors (ALRs). Conceptually, receptors constituting these families are united by two general features. Firstly, they directly recognize common antigen determinants of virtually all classes of pathogens (so-called pathogen-associated molecular patterns, or simply PAMPs) and initiate immune response against them via specific intracellular signaling pathways. Secondly, they recognize endogenous ligands (since they are usually released during cell stress, they are called damage-associated molecular patterns, DAMPs), and, hence, PRR-mediated immune response can be activated without an influence of infectious agents. So, pattern recognition receptors play the key role performing the innate and adaptive immune response. In addition, many PRRs have a number of other vital functions apart from participation in immune response realization. The fundamental character and diversity of PRR functions have led to amazingly rapid research in this field. Such investigations are very promising for medicine as immune system plays a key role in vast majority if not all human diseases, and the process of discovering the new aspects of the immune system functioning is rapidly ongoing. The role of Toll-like receptors in cancer was analyzed in certain reviews but the data are still scattered. This collection of reviews systematizes the key information in the field.
Toll-Like Receptors --- C-type lectin receptors --- nod-like receptors --- DNA Repair --- Pattern Recognition Receptors --- Inflammation --- RIG-I-like receptors --- Autophagy --- Cancer --- Apoptosis
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The innate immune system is the first line of defense against bacterial and viral infections and sterile inflammation through the recognition of pathogen-associated molecular patterns (PAMPs) by pathogen recognition receptors (PRRs) resulting in the production of proinflammatory and antiviral cytokines and chemokines. Several damage-associated molecular patterns (DAMPs), which were released by passive or active mechanisms under sterile conditions, are additionally recognized by PRRs and can cause or even aggravate the inflammatory response. In this special issue many aspects of innate immunity are summarized. Mechanisms of different DAMPs to induce pro- and anti-inflammatory activities, functions of different immune cells, as well as the crosstalk between coagulation and innate immunity were described. Furthermore, aspects of autoinflammatory diseases, types of programmed cell death pathways, and insect immunity are covered. Finally, therapeutic options for the treatment of diseases related to autoimmunity or infections are suggested. Overall, this special issue presents a broad overview of activities related to sterile inflammation and defense mechanisms of innate immunity.
Medicine --- inflammation --- type I interferons --- interleukin-1β --- crosstalk --- hepatic non-parenchymal cells --- albumin --- chronic liver diseases --- bacteria --- cytomegalovirus --- endothelin receptor --- repurposing --- cell culture --- Drosophila suzukii --- hemocytes --- plasmatocytes --- extracellular traps --- HMGB1 --- RAGE --- TLR4 --- DAMP --- SIRT1 --- α7-nicotinic acetylcholine receptor --- nociceptor --- cancer --- COVID-19 --- proteostasis --- autoinflammation --- ribosomopathies --- proteinopathies --- proteasomopathies --- extracellular RNA --- cytokines --- macrophages --- endothelial cells --- toll-like receptors --- angiogenesis --- γδ T cells --- gamma delta T cells --- proliferation --- macrophage polarization --- neutrophils --- neutrophil extracellular traps --- NETs --- ischemia --- PANoptosis --- PANoptosome --- pyroptosis --- apoptosis --- necroptosis --- inflammatory cell death --- inflammasome --- innate immunity --- infection --- NLR --- caspase --- IRF1 --- ZBP1 --- RIPK1 --- RIPK3 --- MLKL --- NLRP3 --- AIM2 --- Pyrin --- caspase-1 --- ASC --- caspase-8 --- caspase-3 --- caspase-7 --- plasticity --- redundancy --- SMOC1 --- thrombin --- n/a
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Endotoxins are potentially toxic compounds produced by Gram-negative bacteria including some pathogens. Unlike exotoxins, which are secreted in soluble form by live bacteria, endotoxins are comprised of structural components of bacteria. Endotoxins can cause a whole-body inflammatory state, sepsis, leading to low blood pressure, multiple organ dysfunction syndrome and death. This book brings together contributions from researchers in the forefront of these subjects. It is divided into two sections. The first deals with how endotoxins are synthesized and end up on the bacterial surface. The second discussed how endotoxins activate TLR4 and, in turn, how TLR4 generates the molecular signals leading to infectious and inflammatory diseases. The way endotoxins interact with the host cells is fundamental to understanding the mechanism of sepsis, and recent research on these aspects of endotoxins has served to illuminate previously undescribed functions of the innate immune system. This volume presents a description of endotoxins according to their genetic constitution, structure, function and mode of interaction with host cells.
Endotoxins -- Pathophysiology. --- Endotoxins. --- Septic shock -- Molecular aspects. --- Endotoxins --- Septic shock --- Biological Science Disciplines --- Toll-Like Receptors --- Bacterial Toxins --- Receptors, Pattern Recognition --- Toxins, Biological --- Natural Science Disciplines --- Physiology --- Toll-Like Receptor 4 --- Receptors, Immunologic --- Disciplines and Occupations --- Biological Factors --- Receptors, Cell Surface --- Chemicals and Drugs --- Membrane Proteins --- Proteins --- Amino Acids, Peptides, and Proteins --- Biology --- Human Anatomy & Physiology --- Health & Biological Sciences --- Microbiology & Immunology --- Animal Biochemistry --- Pathophysiology --- Molecular aspects --- Bacterial pyrogens --- Endotoxin --- Lipopolysaccharides, Microbial --- Microbial lipopolysaccharides --- Medicine. --- Immunology. --- Medical microbiology. --- Pharmacology. --- Infectious diseases. --- Biomedicine. --- Medical Microbiology. --- Infectious Diseases. --- Pharmacology/Toxicology. --- Bacterial cell walls --- Bacterial toxins --- Gram-negative bacteria --- Microbial lipids --- Microbial polysaccharides --- Pyrogens --- Microbiology. --- Emerging infectious diseases. --- Toxicology. --- Immunobiology --- Life sciences --- Serology --- Chemicals --- Medicine --- Pharmacology --- Poisoning --- Poisons --- Emerging infections --- New infectious diseases --- Re-emerging infectious diseases --- Reemerging infectious diseases --- Communicable diseases --- Microbial biology --- Microorganisms --- Toxicology --- Drug effects --- Medical pharmacology --- Medical sciences --- Chemotherapy --- Drugs --- Pharmacy --- Physiological effect
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Mammalian Toll-like receptors (TLRs) were first identified in 1997 based on their homology with Drosophila Toll, which mediates innate immunity in the fly. In recent years, the number of studies describing TLR expression and function in the nervous system has been increasing steadily and expanding beyond their traditional roles in infectious diseases to neurodegenerative disorders and injury. Interest in the field serves as the impetus for this volume in the Current Topics in Microbiology and Immunology series entitled "Toll-like receptors: Roles in Infection and Neuropathology". The first five chapters highlight more traditional roles for TLRs in infectious diseases of the CNS. The second half of the volume discusses recently emerging roles for TLRs in non-infectious neurodegenerative diseases and the challenges faced in these models with identifying endogenous ligands. Several conceptual theories are introduced in various chapters that deal with the dual nature of TLR engagement and whether these signals favor neuroprotective versus neurodegenerative outcomes. This volume should be informative for both experts as well as newcomers to the field of TLRs in the nervous system based on its coverage of basic TLR biology as well as specialization to discuss specific diseases of the nervous system where TLR function has been implicated. A must read for researchers interested in the dual role of these receptors in neuroinfection and neurodegeneration.
Cell receptors. --- Infection. --- Nervous system -- Diseases. --- Virology. --- Cell receptors --- Nervous system --- Infection --- Virology --- Nervous System Diseases --- Bacterial Infections and Mycoses --- Receptors, Pattern Recognition --- Diseases --- Receptors, Immunologic --- Receptors, Cell Surface --- Membrane Proteins --- Proteins --- Amino Acids, Peptides, and Proteins --- Chemicals and Drugs --- Central Nervous System Diseases --- Toll-Like Receptors --- Neurodegenerative Diseases --- Medicine --- Biology --- Health & Biological Sciences --- Cytology --- Microbiology & Immunology --- Neurology --- Diseases. --- Infectious diseases --- Medical neurology --- Nerves --- Neuropathology --- Cell membrane receptors --- Cell surface receptors --- Receptors, Cell --- Medicine. --- Immunology. --- Neurosciences. --- Parasitology. --- Biomedicine. --- Microbiology --- Neural sciences --- Neurological sciences --- Neuroscience --- Medical sciences --- Immunobiology --- Life sciences --- Serology --- Clinical sciences --- Medical profession --- Human biology --- Pathology --- Physicians --- Medical microbiology --- Neurologic disorders --- Neurological disorders --- Binding sites (Biochemistry) --- Cell membranes --- Causes and theories of causation --- Medical virology. --- Medical parasitology. --- Human beings --- Human parasitology --- Parasitology --- Parasitic diseases --- Virus diseases --- Parasites
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Our common knowledge on oxidative stress has evolved substantially over the years and has been mostly focused on the fundamental chemical reactions and the most relevant chemical species involved in the human pathophysiology of oxidative stress-associated diseases. Thus, reactive oxygen species and reactive nitrogen species (ROS and RNS) were identified as the key players initiating, mediating, and regulating the cellular and biochemical complexity of oxidative stress either as physiological (acting pro-hormetic) or as pathogenic (causing destructive vicious circle) process. The papers published in this particular Special Issue of the Cells demonstrate the impressive pathophysiological relevance of ROS and RNS in a range of contexts, including the relevance of second messengers of free radicals like 4-hydroxynonenal, allowing us to assume that even more detailed mechanisms of their positive and negative effects lie in wait, and should assist in better monitoring of the major modern diseases and the development of advanced integrative biomedicine treatments.
toxicity --- toll-like receptors --- acrolein --- hydroxyapatite-based biomaterials --- LC-MS/MS --- blood–brain barrier --- NADPH-oxidase --- human neuroblastoma SH-SY5Y cells --- NRF2-NQO1 axis --- granulocytes --- free radicals --- antioxidant --- plaque vulnerability --- bEnd.3 --- relaxation --- Ca2+ --- keratinocytes --- oxidative metabolism of the cells --- lipid peroxidation --- intermittent hypoxia --- osteoblast growth --- UV radiation --- ROS --- bEnd5 --- cyclopurines --- NF?B --- glucose deprivation --- antimicrobial --- endothelial cells --- 4-hydroxynonenal (4-HNE) --- histamine --- glutamine deprivation --- optical coherence tomography --- antioxidants --- DNA damage --- glutathione --- NQO1 transcript variants --- xeroderma pigmentosum --- cancer cells --- VAS2870 --- reactive oxygen species (ROS) --- TP53 mutation --- DNA and RNA polymerases --- viability --- oxidative burst --- macrophages --- inflammation --- Nrf2 --- von Willebrand factor --- reactive oxygen species --- growth control --- intracellular signaling --- MFN2 --- nuclear factor erythroid 2–related factor 2 --- fusion/fission --- IMR-90 --- calcium --- proliferation --- mitochondria --- pathophysiology of oxidative stress --- redox balance --- 4-hydroxynonenal --- cannabidiol --- oxidative homeostasis --- rs1800566 --- neuronal cell death --- heme-oxygenase-1 --- vitamins --- cell signaling --- TRPM2 channel --- aorta --- cancer --- growth --- cancer regression --- oxidative stress --- nucleotide excision repair
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This book is a compilation of articles by experts on the prevention and treatment of periodontal disease, many of which are full of data-based evidence from basic research perspectives or patient data.
70-kDa heat shock proteins --- gingival crevicular fluid --- heat shock protein --- periodontitis --- periodontal disease --- diabetes --- diabetic retinopathy --- bleeding on probing --- probing pocket depth --- fasting blood sugar --- carotid artery calcification --- alveolar bone loss --- computed tomography --- panoramic radiographs --- aspiration pneumonia --- chronic periodontitis --- Porphyromonas gingivalis --- proinflammatory cytokines --- TLR2 --- epidemiological index --- item response theory --- oral examination --- diagnosis --- Mfa1 --- Toll-like receptors --- gingival fibroblast --- azithromycin --- human gingival fibroblast --- human periodontal ligament fibroblast --- IL-6 --- IL-8 --- MMP-1 --- MMP-2 --- chewing ability --- infection --- inflammation --- periodontal medicine --- Gan-Lu-Yin --- herbal medicine --- osteoclastogenesis --- periodontal diseases --- periodontal pocket --- health status indicators --- periodontal inflamed surface area (PISA) --- rheumatoid arthritis --- tocilizumab --- periodontal inflamed surface area --- periodontal pathogen --- mixed effect modeling --- follow-up study --- Low reactive Level Laser Therapy (LLLT) --- human gingival fibroblasts (HGF) --- microarray --- differentially gene expression (DEGs) --- gene ontology --- biological processes (BP) --- protein–protein interaction (PPI)
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Creatine plays a critical role in cellular metabolism, primarily by binding with phosphate to form phosphocreatine (PCr) as well as shuttling high-energy phosphate compounds in and out of the mitochondria for metabolism. Increasing the dietary availability of creatine increases the tissue and cellular availability of PCr, and thereby enhances the ability to maintain high-energy states during intense exercise. For this reason, creatine monohydrate has been extensively studied as an ergogenic aid for exercise, training, and sport. Limitations in the ability to synthesize creatine and transport and/or store dietary creatine can impair metabolism and is a contributor to several disease states. Additionally, creatine provides an important source of energy during metabolically stressed states, particularly when oxygen availability is limited. Thus, researchers have assessed the role of creatine supplementation on health throughout the lifespan, as well as whether creatine availability may improve disease management and/or therapeutic outcomes. This book provides a comprehensive overview of scientific and medical evidence related to creatine's role in metabolism, health throughout the lifespan, and our current understanding of how creatine can promote brain, heart, vascular and immune health; reduce the severity of musculoskeletal and brain injury; and may provide therapeutic benefits in glucose management and diabetes, cancer therapy, inflammatory bowel disease, and post-viral fatigue.
ergogenic aids --- cellular metabolism --- phosphagens --- sarcopenia --- cognition --- diabetes --- creatine synthesis deficiencies --- concussion --- traumatic brain injury --- spinal cord injury --- muscle atrophy --- rehabilitation --- pregnancy --- immunity --- anti-inflammatory --- antioxidant --- anticancer --- creatine --- nutritional supplements --- fertility --- newborn --- development --- brain injury --- post-viral fatigue syndrome --- chronic fatigue syndrome --- GAA --- creatine kinase --- dietary supplements --- exercise --- skeletal muscle --- glycemic control --- type 2 diabetes mellitus --- phosphorylcreatine --- dietary supplement --- ergogenic aid --- youth --- athletes --- osteoporosis --- osteosarcopenia --- frailty --- cachexia --- innate immunity --- adaptive immunity --- inflammation --- macrophage polarization --- cytotoxic T cells --- toll-like receptors --- vascular pathology --- cardiovascular disease --- oxidative stress --- vascular health --- female --- menstrual cycle --- hormones --- exercise performance --- menopause --- mood --- children --- height --- BMI-for-age --- stature-for-age --- growth --- phosphocreatine --- creatine transporter --- supplementation --- treatment --- heart --- heart failure --- ischemia --- myocardial infarction --- anthracycline --- cardiac toxicity --- energy metabolism --- cell survival --- bioinformatics --- systems biology --- cellular allostasis --- dynamic biosensor --- pleiotropic effects of creatine (Cr) supplementation --- inflammatory bowel diseases (IBD) --- ulcerative colitis --- Crohn’s disease --- creatine kinase (CK) --- phosphocreatine (PCr) --- creatine transporter (CrT) --- intestinal epithelial cell protection --- intestinal tissue protection --- creatine perfusion --- organ transplantation --- Adenosine mono-phosphate (AMP) --- activated protein kinase (AMPK) --- liver kinase B1 (LKB1) --- mitochondrial permeability transition pore (mPTP) --- reactive oxygen species (ROS) --- glucose transporter (GLUT) --- T cell antitumor immunity --- metabolic regulator --- cancer immunotherapy --- supplements --- muscle damage --- recovery --- immobilization --- atrophy --- muscular dystrophy --- amyotrophic lateral sclerosis --- Parkinson’s Disease --- cardiopulmonary disease --- mitochondrial cytopathy --- hypertrophy --- athletic performance --- weightlifting --- resistance exercise --- training --- muscular power --- muscular adaptation --- muscle fatigue --- adipose tissue --- muscle strength --- physiological adaptation --- mitochondria --- thermogenesis --- MAP kinase signaling system --- sodium-chloride-dependent neurotransmitter symporters --- signal transduction --- intradialytic creatine supplementation --- hemodialysis --- muscle --- protein energy wasting --- clinical trial --- muscle weakness --- chronic fatigue --- cognitive impairment --- depression --- anemia --- resistance training --- sports nutrition --- strength --- toxicity --- methylation --- hyperhomocysteinemia --- neuromodulation --- MCDA --- mitochondriopathia --- cardiac infarction --- long COVID --- hypoxia --- stroke --- neurodegenerative diseases --- noncommunicable disease --- adenosine 5′-monopnophosphate-activated protein kinase --- anthracyclines --- creatine supplementation --- cardiac signaling --- cardiotoxicity --- doxorubicin --- soy --- vegetarian/vegan diet --- amino acids --- dietary ingredients --- performance
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