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Microbial Modulation of Host Apoptosis and Pyroptosis

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889192809 Year: Pages: 109 DOI: 10.3389/978-2-88919-280-9 Language: English
Publisher: Frontiers Media SA
Subject: Internal medicine --- Science (General)
Added to DOAB on : 2015-12-10 11:59:06
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Abstract

Infectious disease is the result of an interactive relationship between a microbial pathogen and its host. In this interaction both the host and the pathogen attempt to manipulate each other using a complex network to maximize their respective survival probabilities. Programmed host cell death is a direct outcome of host-pathogen interaction and may benefit host or pathogen depending on microbial pathogenesis. Apoptosis and pyroptosis are two common programmed cell death types induced by various microbial infections. Apoptosis is non-inflammatory programmed cell death and can be triggered through intrinsic or extrinsic pathways and with or without the contribution of mitochondria. Pyroptosis is an inflammatory cell death and is typically triggered by caspase-1 after its activation by various inflammasomes. However, some non-canonical caspase-1-independent proinflammatory cell death phenomena have been reported. Microbial pathogens are able to modulate host apoptosis and pyroptosis through different triggers and pathways. The promotion and inhibition of host apoptosis and pyroptosis vary and depend on the microbe types, virulence, and phenotypes. For example, virulent pathogens and attenuated vaccine strains may use different pathways to modulate host cell death. Specific microbial genes may be responsible for the modulation of host cell death. Different host cells, including macrophages, dendritic cells, and T cells, can undergo apoptosis and pyroptosis after microbial infections. The pathways of host apoptosis and pyroptosis induced by different microbes may also differ. Different methods can be used to study the interaction between microbes and host cell death system. The articles included in this E-book report the cutting edge findings in the areas of microbial modulation of host apoptosis, pyroptosis and inflammasome.

Marine Anti-inflammatory Agents

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ISBN: 9783039215720 9783039215737 Year: Pages: 248 DOI: 10.3390/books978-3-03921-573-7 Language: English
Publisher: MDPI - Multidisciplinary Digital Publishing Institute
Subject: Medicine (General)
Added to DOAB on : 2019-12-09 11:49:16
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Abstract

Acute inflammation is a highly regulated process, and its dysregulation can lead to the development of a chronic inflammatory state which is believed to play a main role in the pathogenesis of many diseases, including cancer. In recent years, the need to find new anti-inflammatory molecules has raised the scientific community´s interest for marine natural products. In this regard, the marine environment represents a source for isolating a wealth of bioactive compounds. In this Special Issue, the reported products have been obtained from microalgae, sea cucumber, octopus, squid, red alga-derived fungus, cnidarians, hard-shelled mussel, and sponges.

Keywords

THP-1 macrophages --- anti-inflammatory --- TLR4 --- NF-?B --- MAPK --- SPR analysis --- glycolipids --- MGDG --- skin --- inflammation --- epidermal hyperplasia --- microalgae --- Isochrysis galbana --- Frondanol --- Cucumaria frondosa --- DSS colitis --- colon inflammation --- zoantharia --- Tropical Eastern Pacific --- Zoanthus pulchellus --- zoanthamine --- inflammation --- fucoxanthin --- inflammation --- epidermal hyperplasia --- UVB --- photoprotection --- 6-bromoindole --- Geodia barretti --- anti-inflammatory activity --- dendritic cells --- T cell differentiation --- poor blood circulation --- Ecklonia cava --- phlorotannins --- pyrogallol-phloroglucinol-6,6-bieckol --- functional ingredients --- endothelial cell death --- vascular smooth muscle cell proliferation and migration --- inflammation --- anti-inflammatory --- bioactive molecules --- microalgae --- polysaccharides --- carotenoids --- polyunsaturated fatty acids --- fucoxanthin --- ultraviolet B --- denervation --- seafood waste --- polyunsaturated fatty acid --- NO inhibition --- fish oil --- marine nutraceuticals --- fish oil --- omega-3 --- eicosapentaenoic acid --- docosahexaenoic acid --- inflammation --- eicosanoid --- cytokine --- surgery --- critical illness --- parenteral nutrition --- signal transducer and activator of transcription 3 (STAT3) --- matrix metalloproteinases-9 (MMP-9) --- interleukin (IL) --- lipopolysaccharide (LPS) --- acute sickness behavior --- acute lung injury (ALI) --- prostaglandins --- clavulones --- punaglandins --- thromboxane --- inflammation --- marine vertebrates --- marine invertebrates --- diatoms --- macroalgae --- fucoxanthin --- rosmarinic acid --- NRLP3 --- inflammasome --- anti-oxidative --- anti-inflammatory --- photo-protection --- UVB

Kidney Inflammation, Injury and Regeneration

Authors: --- ---
ISBN: 9783039285389 / 9783039285396 Year: Pages: 496 DOI: 10.3390/books978-3-03928-539-6 Language: eng
Publisher: MDPI - Multidisciplinary Digital Publishing Institute
Subject: Medicine (General) --- Internal medicine
Added to DOAB on : 2020-06-09 16:38:57
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Abstract

Acute kidney injury (AKI) is still associated with high morbidity and mortality incidence rates, and also bears an elevated risk of subsequent chronic kidney disease. Although the kidney has a remarkable capacity for regeneration after injury and may recover completely depending on the type of renal lesions, the options for clinical intervention are restricted to fluid management and extracorporeal kidney support. The development of novel therapies to prevent AKI, to improve renal regeneration capacity after AKI, and to preserve renal function is urgently needed. The Special Issue covers research articles that investigated the molecular mechanisms of inflammation and injury during different renal pathologies, renal regeneration, diagnostics using new biomarkers, and the effects of different stimuli like medication or bacterial components on isolated renal cells or in vivo models. The Special Issue contains important reviews that consider the current knowledge of cell death and regeneration, inflammation, and the molecular mechanisms of kidney diseases. In addition, the potential of cell-based therapy approaches that use mesenchymal stromal/stem cells or their derivates is summarized. This edition is complemented by reviews that deal with the current data situation on other specific topics like diabetes and diabetic nephropathy or new therapeutic targets.

Keywords

kidney injury --- alport syndrome --- modifier gene --- nephrin --- podocin --- glomerular basement membrane --- slit diaphragm --- focal segmental glomerulosclerosis --- inflammatory bowel disease (IBD) --- DSS-colitis --- glomerular filtration barrier (GFB) --- type IV collagen --- type I collagen --- type V collagen --- genotype --- IL-18 --- polymorphism --- renal cell carcinoma --- Taiwan --- mesenchymal stem cells --- acute and chronic kidney disease --- exosome --- natural products --- non-coding RNAs --- microRNAs --- long non-coding RNAs --- renal fibrosis --- biomarkers --- therapeutics targets --- rhabdomyolysis --- pigment nephropathy --- haem --- NLRP3 inflammasome --- acute kidney injury --- hypertension --- kidney --- molecular signaling --- hematuria --- inflammation --- oxidative stress --- tubular injury --- AKI --- chronic kidney disease (CKD) --- mesenchymal stromal cells --- extracellular vesicles --- acute kidney injury --- modified-MSCs --- microRNA --- mesenchymal stem cell --- mesodermal stem cell --- renal ischemia-reperfusion --- inflammation --- kidney transplantation --- microRNA --- extracellular vesicles --- exosomes --- B-cell attracting chemokine --- CXCL13 --- kidney transplantation --- allograft rejection --- T cell-mediated rejection --- diabetic nephropathy --- lysophosphatidic acid --- lysophosphatidic acid receptor --- chronic kidney injury --- kidney proximal tubule --- acute kidney failure --- signal transduction --- transcription --- CREB Regulated Transcriptional Coactivators (CRTC) --- cAMP Regulatory Element Binding Protein (CREB) --- Salt Inducible Kinase (SIK) --- Class IIa Histone Deacetylases (HDAC) --- lncRNA --- long non-coding RNA --- miRNA --- kidney --- glomerulus --- podocyte --- acute kidney injury --- AKI --- diabetic nephropathy --- diabetic kidney disease --- diabetic nephropathy --- inflammation --- signaling cascade --- ischemia-reperfusion --- acute kidney injury --- stem cell --- conditioned medium --- inflammation --- apoptosis --- necrosis --- regulated necrosis --- kidney injury --- tubular injury --- glomerular injury --- polyunsaturated fatty acids --- omega-3 fatty acid --- inflammatory maker --- C-reactive protein --- interleukin-6 --- LPS-binding protein --- fibrosis --- pericyte --- myofibroblast --- endotoxemia-induced oliguric kidney injury --- arachidonic acid --- cyclooxygenase --- lipoxygenase --- cytochrome P450 --- kidney inflammation --- therapeutic target --- obese kidney fibrosis --- endotoxemia --- ROS --- cPLA2 and COX-2 --- IgA nephropathy --- KIT assay --- KIT-IgA score --- noninvasive --- diagnostics --- prediction --- diabetic kidney diseases --- xanthine oxidase --- glomerular damage --- acute kidney injury --- chronic kidney disease --- renal progenitors --- polyploidization --- diabetic nephropathy --- diabetes mellitus --- GLP-1 receptor agonists --- SGLT2 inhibitors --- molecular mechanisms --- chemerin --- CmklR1 --- 2-kidney-1-clip --- 2k1c --- Thy1.1 nephritis --- renovascular hypertension --- renal inflammation --- renal injury --- renal fibrosis --- inflammation --- ischemia/reperfusion injury --- Farnesiferol B --- Nuclear Factor kappa-light-chain-enhancer of activated B cells (NF-?B) --- G-protein-coupled bile acid receptor (TGR5) --- renal stem cells --- differentiation --- scattered tubular cells --- papilla --- niches --- renal tubular cells --- epithelial cells --- proximal tubule --- cytotoxicity --- injury --- inflammation --- empagliflozin --- dapagliflozin --- kidney --- n/a

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