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Secretion of Cytokines and Chemokines by Innate Immune Cells

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889195503 Year: Pages: 134 DOI: 10.3389/978-2-88919-550-3 Language: English
Publisher: Frontiers Media SA
Subject: Allergy and Immunology --- Medicine (General)
Added to DOAB on : 2016-01-19 14:05:46
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The release of cytokines, chemokines, and other immune-modulating mediators released from innate immune cells, including eosinophils, neutrophils, macrophages, dendritic cells, mast cells, and epithelial cells, is an important event in immunity. Cytokine synthesis and transportation occurs through the canonical protein trafficking pathway associated with endoplasmic reticulum and Golgi. How cytokines are released upon their exit from the trans-Golgi network varies enormously between cell types, and in many cells this has not yet been characterized. This issue delves into the plethora of cytokines released by innate immune cells, and where possible, shines light on specific mechanisms that regulate trafficking and release of Golgi-derived vesicles. Each cell type also shows varying degrees of dependency on microtubule organization and actin cytoskeleton remodeling for cytokine secretion. Understanding the mechanisms of cytokine secretion will reveal the inner workings of individual innate immune cell types, and allow identification of critical regulatory steps in cytokine release.

Thymic stromal alterations and genetic disorders of immune system

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889197170 Year: Pages: 81 DOI: 10.3389/978-2-88919-717-0 Language: English
Publisher: Frontiers Media SA
Subject: Allergy and Immunology --- Medicine (General)
Added to DOAB on : 2016-04-07 11:22:02
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The pathogenic mechanisms underlying primary T-cell disorders are mainly related to molecular alterations of genes whose expression is intrinsic to hematopoietic cells. However, since the differentiation process requires a crosstalk among thymocytes and the thymic microenvironment, molecular alterations of genes, involved in the differentiation and functionality of the stromal component of the thymus, may lead to a severe T-cell defect or failure of central tolerance, as well. The first example of severe combined immunodeficiency (SCID) not related to an intrinsic alteration of the hematopoietic cell but rather of the thymic epithelial component is the Nude/SCID phenotype, inherited as an autosomal recessive disorder, whose hallmarks are the T-cell defect and the absence of the thymus. The clinical and immunological phenotype is the human equivalent of the murine Nude/SCID syndrome, which represents the first spontaneous SCID identified in nude mice in 1966. For over 3 decades studies of immune system in these mice enormously contributed to the overall knowledge of cell mediated immunity, in the assumption that the athymia of these mice was solely responsible for the T-cell immunological defect. This syndrome is due to mutations of the transcription factor FOXN1, belonging to the forkhead-box gene family, which is mainly expressed in the thymus and skin epithelial cells, where it plays a critical role in differentiation and survival. An alteration of the thymic structure is also a feature of the DiGeorge syndrome (DGS), which has been long considered the human counterpart of the nude mice phenotype. This syndrome is frequently associated to a deletion of the 22q11 region, which contains approximately 30 genes, including the TBX1 gene, which is responsible for most of the clinical features of DGS in humans and mice. In this syndrome common manifestations are cardiac malformations, speech delay, hypoparathyrodism and immunodeficiency, even though the immunological hallmarks of the T-cell defect in DiGeorge syndrome are profoundly different from those reported in human Nude/SCID. The divergence of the phenotype among these 2 entities raised the possibility that the FOXN1 transcription factor represents the real key stromal molecule implicated in directing the hematopoietic stem cell toward a proper T-cell fate. Thymic stromal component of the primary lymphoid organ is also required to negatively select the autoreactive clones, a process driven by the expression of tissue specific antigens (TSA) by medullary thymic epithelial cells (mTECs). The expression of genes encoding TSA antigens is mediated by autoimmune regulator (AIRE) gene, encoding a transcription factor expressed in mTECs. Molecular alterations of this gene are associated to autoimmune polyendocrinopathy candidiasis ectodermal dystrophy (APECED), a rare autosomal disorder, which may be considered the prototype of an autoimmune disease due to the failure of central tolerance homeostasis. All these "experiments of nature" led to unravel novel pathogenic mechanisms underlying inherited disorders of immune system and, of note, to clarify the pivotal role of epithelial cells in the maturation and education process of T-cell precursors.

Effects of Mycotoxins on the Intestine

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ISBN: 9783038977827 9783038977834 Year: Pages: 262 DOI: 10.3390/books978-3-03897-783-4 Language: eng
Publisher: MDPI - Multidisciplinary Digital Publishing Institute
Subject: Medicine (General) --- Public Health
Added to DOAB on : 2019-05-09 17:16:14
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Abstract

Mycotoxins are secondary metabolites produced by several fungal species. They can contaminate human food and animal feed, and have been a threat for thousands of years. The gastrointestinal tract is the first target when ingesting mycotoxin-contaminated food or feed. As unlikely as it sounds, the investigations concerning the effects of mycotoxins on the intestine are still in their early stages. This book gathers the most recent advances related to the characterization of the intestinal toxicity of mycotoxins. Substantial data assembled on the damage caused to a number of histological structures and functions of the intestine remove any remaining doubt about this organ being a primary target for the toxicity of mycotoxins. An interesting overview of the detrimental effects of mycotoxins on the gut-hosted microbiota—now regarded as a fully-fledged organ associated with the gut—is also given. Finally, outstanding contributions in this book address questions relating to the suitability of current regulations to protect against alterations of the intestine, and to the efficacy assessment of new detoxification strategies using the intestinal toxicity of mycotoxins as a relevant endpoint.

Keywords

mice --- aflatoxin B1 --- intestinal bacterial flora --- response --- Clostridium sp. WJ06 --- deoxynivalenol --- pig --- intestinal morphology --- microbial diversity --- aflatoxin M1 --- ochratoxin A --- intestinal epithelial cells --- tight junction --- permeability --- ileum --- jejunum --- deoxynivalenol --- piglet --- contaminated feed --- tight junction --- aflatoxin B1 --- small intestine --- histopathological lesions --- ultrastructural changes --- toll-like receptors --- T-2 toxin --- enteric nervous system --- pig --- vasoactive intestinal polypeptide --- mycotoxins --- zearalenone --- deoxynivalenol --- histology --- ultrastructure --- large intestine --- pig --- Claviceps --- liver --- digestive tract --- mycotoxin --- sclerotia --- ergot alkaloids --- toxicity --- deoxynivalenol --- Saccharomyces cerevisiae boulardii CNCM I-1079 --- intestine --- transcriptome --- inflammation --- oxidative stress --- lipid metabolism --- fumonisin --- microbiota --- pigs --- MiSeq 16S rDNA sequencing --- intestinal microbiota --- hydrogen-rich water --- lactulose --- Fusarium mycotoxins --- piglets --- functional oligosaccharides --- mycotoxins --- swine --- explant technique --- intestinal morphology --- goblet cells --- deoxynivalenol --- zearalenone --- pig --- colon microbiota --- Lactobacillus --- detoxification --- zearalenone --- doses --- caecal water --- genotoxicity --- pre-pubertal gilts --- atlantic salmon --- deoxynivalenol --- feed --- intestine --- PCR --- proliferating cell nuclear antigen --- suppressor of cytokine signaling --- tight junctions --- Zearalenone --- N-acetylcysteine --- SIEC02 cells --- Mitochondrial apoptosis --- n/a

AMP-Activated Protein Kinase Signalling

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ISBN: 9783038976622 Year: Pages: 452 DOI: 10.3390/books978-3-03897-663-9 Language: eng
Publisher: MDPI - Multidisciplinary Digital Publishing Institute
Subject: Science (General) --- Biology
Added to DOAB on : 2019-03-21 14:08:22
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Abstract

Starting from a kinase of interest, AMP-activated protein kinase (AMPK) has gone far beyond an average biomolecule. Being expressed in all mammalian cell types and probably having a counterpart in every eukaryotic cell, AMPK has attracted interest in virtually all areas of biological research. Structural and biophysical insights have greatly contributed to a molecular understanding of this kinase. From good old protein biochemistry to modern approaches, such as systems biology and advanced microscopy, all disciplines have provided important information. Thus, multiple links to cellular events and subcellular localizations have been established. Moreover, the crucial involvement of AMPK in human health and disease has been evidenced. AMPK accordingly has moved from an interesting enzyme to a pharmacological target. However, despite our extensive current knowledge about AMPK, the growing community is busier than ever. This book provides a snapshot of recent and current AMPK research with an emphasis on work providing molecular insight, including but not limited to novel physiological and pathological functions, or regulatory mechanisms. Up-to-date reviews and research articles are included.

Keywords

exercise --- glucose uptake --- AMP-activated protein kinase --- TBC1D4 --- AS160 --- AMP-activated protein kinase --- developmental origins of health and disease (DOHaD) --- hypertension --- kidney disease --- nutrient-sensing signals --- oxidative stress --- renin-angiotensin system --- AMPK --- autophagy --- co-expression --- microarrays --- 3T3-L1 --- adipocyte --- differentiation --- AMPK --- tight junctions --- epithelial cells --- ZO-1 --- par complex --- MDCK --- nectin-afadin --- adherent junctions --- TAK1 --- AMPK --- phosphorylation --- AMPK kinase --- endothelial nitric-oxide synthase --- vasodilation --- phenylephrine --- vasoconstriction --- endothelial cells --- ionomycin --- AMPK --- liver --- lipid metabolism --- fatty acid oxidation --- indirect calorimetry --- atrophy --- regrowth --- sirtuin 1 (SIRT1) --- peroxisome proliferator-activated receptor gamma coactivator 1-? (PGC1?) --- heat shock protein --- fiber-type --- AMPK --- monocytes --- macrophages --- differentiation --- autophagy --- AML --- MDS --- CML --- CMML --- pregnancy --- catechol-O-methyltransferase --- 2-methoxyestradiol --- preeclampsia --- gestational diabetes mellitus --- AMPK --- IL-1? --- NLRP3 --- nutrition --- dietary fatty acids --- metabolic-inflammation --- nutrigenomics --- AMPK --- LKB1 --- autophagy --- proteasome --- hypertrophy --- atrophy --- skeletal muscle --- AICAR --- mTOR --- protein synthesis --- AMPK --- epigenetics --- chromatin remodeling --- histone modification --- DNA methylation --- medulloblastoma --- sonic hedgehog --- AMPK --- AMP-activated protein kinase (AMPK) --- spermatozoa --- motility --- mitochondria --- membranes --- signaling --- stress --- assisted reproduction techniques --- AMP-activated protein kinase --- epigenetics --- protein acetylation --- KATs --- HDACs --- acetyl-CoA --- NAD+ --- AMP-activated protein kinase --- glycogen --- exercise --- metabolism --- cellular energy sensing --- energy utilization --- liver --- skeletal muscle --- metabolic disease --- glycogen storage disease --- resveratrol --- AMPK --- hepatocyte --- liver --- steatosis --- transporter --- carrier --- pump --- membrane --- energy deficiency --- AMPK --- infection --- mycobacteria --- host defense --- energy metabolism --- AMPK --- activation loop --- AID --- ?-linker --- ?-linker --- CBS --- LKB1 --- CaMKK2 --- ?RIM --- hypothalamus --- adenosine monophosphate-activated protein kinase --- adipose tissue --- food intake --- adaptive thermogenesis --- beiging --- AMPK --- HDAC4/5 --- p70S6K --- MyHC I(?), motor endplate remodeling --- soleus muscle --- mechanical unloading --- hindlimb suspension --- AMPK --- synaptic activation --- PKA --- CREB --- soluble Adenylyl cyclase --- Immediate early genes --- transcription --- AMPK --- autophagy --- metabolism --- mTOR --- ULK --- AMP-activated protein kinase --- protein kinase B --- Akt --- insulin signalling --- A769662 --- endothelial function --- n/a

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