Search results for "inflammation"
showing 10 items of 2662 documents
Meta-Analysis of Genome-Wide Association Studies in >80 000 Subjects Identifies Multiple Loci for C-Reactive Protein Levels
2011
Background— C-reactive protein (CRP) is a heritable marker of chronic inflammation that is strongly associated with cardiovascular disease. We sought to identify genetic variants that are associated with CRP levels. Methods and Results— We performed a genome-wide association analysis of CRP in 66 185 participants from 15 population-based studies. We sought replication for the genome-wide significant and suggestive loci in a replication panel comprising 16 540 individuals from 10 independent studies. We found 18 genome-wide significant loci, and we provided evidence of replication for 8 of them. Our results confirm 7 previously known loci and introduce 11 novel loci that are implicated in p…
P-01MicroRNA PROFILING IDETIFY NEW REGULATORY GENES IN ETHANOL-INDUCED NEUROINFLAMMATION AND BRAIN DAMAGE THROUGH TLR4 RECEPTORS
2015
MicroRNAs (miRNAs) are small non-protein coding RNA regulating the transcription and translation of other RNA and are involved in several diseases and disorders, including neurodegeneration. We aim to evaluate the impact of miRNAs in the regulation of ethanol-induced neuro-inflammation and brain damage and to assess the potential role of miRNAs …
Adult Neural Stem Cells Are Alerted by Systemic Inflammation through TNF-α Receptor Signaling.
2021
Summary Adult stem cells (SCs) transit between the cell cycle and a poorly defined quiescent state. Single neural SCs (NSCs) with quiescent, primed-for-activation, and activated cell transcriptomes have been obtained from the subependymal zone (SEZ), but the functional regulation of these states under homeostasis is not understood. Here, we develop a multilevel strategy to analyze these NSC states with the aim to uncover signals that regulate their level of quiescence/activation. We show that transitions between states occur in vivo and that activated and primed, but not quiescent, states can be captured and studied in culture. We also show that peripherally induced inflammation promotes a …
Corrigendum to “Inhibition of neutral endopeptidase (NEP) facilitates neurogenic inflammation” [Exp. Neurol. 195 (2005) 179–184]
2006
Neurogenic Inflammation in Complex Regional Pain Syndrome (CRPS)
2008
This chapter explains symptoms and nature of neurogenic inflammation and its importance in posttraumatic complex regional pain syndrome (CRPS). Neurogenic inflammation regularly accompanies excitation of primary afferent nociceptors. It has two major components – plasma extravasation and vasodilatation. The most important mediators are the neuropeptides calcitonin gene-related peptide (CGRP) and substance P (SP). After peripheral trauma, immune reaction (e.g., cytokines) and the attempts of the tissue to regenerate (e.g., growth factors) sensitize nociceptors and thereby amplify neurogenic inflammation. This cascade of events has recently been demonstrated in rat models of CRPS employing di…
OP0193 Inflammation of adventitial nerves occurs in giant cell arteritis patients and it is characterized by inflammasomes, upr and autophagy activat…
2017
Background Vascular adventitia is a major site of immune surveillance and inflammatory cell trafficking and is the most complex compartment of the vessel wall comprising fibroblasts, dendritic cells and macrophages, progenitor cells, vasa vasorum, pericytes and adrenergic nerves. It has been proposed that activation of adventitial nerves and release of sensory neuropeptides from their peripheral terminals may leads to neurogenic inflammation. Giant cell arteritis (GCA) is an immune-mediated disease of unknown etiology in which the inflammatory process seems to start from the adventitia of affected arteries. Objectives aim of the study was to evaluate the occurrence of adventitial nerves inf…
Homeostasis of Microglia in the Adult Brain: Review of Novel Microglia Depletion Systems.
2015
Microglia are brain macrophages that emerge from early erythro-myeloid precursors in the embryonic yolk sac and migrate to the brain mesenchyme before the blood brain barrier is formed. They seed the brain, and proliferate until they have formed a grid-like distribution in the central nervous system that is maintained throughout lifespan. The mechanisms through which these embryonic-derived cells contribute to microglia homoeostasis at steady state and upon inflammation are still not entirely clear. Here we review recent studies that provided insight into the contribution of embryonically-derived microglia and of adult 'microglia-like' cells derived from monocytes during inflammation. We ex…
Multiple sclerosis – candidate mechanisms underlying CNS atrophy
2009
Recently it has become clear that the neuronal compartment plays a more important role than previously thought in the pathology of multiple sclerosis. Apart from demyelination, neuronal pathology is apparently largely responsible for the brain atrophy that can be observed early on and throughout the course of the disease. The loss of axons and their neurons in the course of chronic neuroinflammation is a major factor determining long-term disability in patients. The actual steps leading from immune attack against the myelin sheath to neuronal damage are not yet fully clear. Here we review key findings about direct axonal damage processes, demyelination-related neuronal pathology and cell-bo…
Ethanol intake in male mice exposed to social defeat: Environmental enrichment potentiates resilience
2021
Large preclinical evidence shows that exposure to social defeat (SD) increases vulnerability to drug abuse, increasing the consumption of ethanol. However, not all subjects are equally affected by the changes induced by stress. Previous reports have evidenced that the resilient phenotype to depressive-like behaviors after SD is associated with the resistant phenotype to cocaine-increased rewarding effects and the smaller neuroinflammatory response. The aim of the present study was to further clarify whether the resilient profile to depressive-like behavior also predicts a protection against the increase in ethanol intake induced by SD. The neuroinflammatory profile was studied after the end…
Mildronate and its neuroregulatory mechanisms: targeting the mitochondria, neuroinflammation, and protein expression.
2013
This review for the first time summarizes the data obtained in the neuropharmacological studies of mildronate, a drug previously known as a cardioprotective agent. In different animal models of neurotoxicity and neurodegenerative diseases, we demonstrated its neuroprotecting activity. By the use of immunohistochemical methods and Western blot analysis, as well as some selected behavioral tests, the new mechanisms of mildronate have been demonstrated: a regulatory effect on mitochondrial processes and on the expression of nerve cell proteins, which are involved in cell survival, functioning, and inflammation processes. Particular attention is paid to the capability of mildronate to stimulate…