Promotion of microglial phagocytosis by tuftsin stimulates remyelination in experimental autoimmune encephalomyelitis.

Promotion of microglial phagocytosis by tuftsin stimulates remyelination in experimental autoimmune encephalomyelitis. Mol Med Rep. 2019 Oct 31;: Authors: Bao Z, Hao J, Li Y, Feng F Abstract Microglia were once thought to serve a pathogenic role in demyelinating diseases, particularly in multiple sclerosis (MS). However, it has recently been shown that in the experimental autoimmune encephalomyelitis (EAE) model of MS, microglia could serve a protective role by promoting remyelination via the efficient removal of apoptotic cells, the phagocytosis of debris and the support of myelinating oligodendrocytes. The aim of the present study was to determine if the effect of microglia could promote the recovery of EAE and attenuate symptoms in EAE. The severity of EAE was assessed by clinical scores, pathologic changes revealed by luxol fast blue staining and immunohistochemical techniques. The results suggested that microglia reduced clinical scores in mice, suppressed ongoing severe EAE and promoted remyelination and recovery in EAE mice. In addition, following induction with tuftsin, the M1/M2 cytokine balance was shifted, downregulating the proinflammatory M1 response and upregulating the anti‑inflammatory M2 response. Generally, microglia can stimulate remyelination, which serves a protective role in different phases of EAE and may represent a potential therapeutic strategy for the treatment of MS. PMID: 31702807 [PubMed - as supplied by publisher]
Source: Molecular Medicine Reports - Category: Molecular Biology Tags: Mol Med Rep Source Type: research

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Publication date: Available online 13 December 2019Source: Brain, Behavior, and ImmunityAuthor(s): N.B. Teixeira, M.B. Sant'Anna, A.C. Giardini, L.P. Araujo, L.A. Fonseca, A.S. Basso, Y. Cury, G. PicoloAbstractMultiple sclerosis (MS) is a Central Nervous System inflammatory demyelinating disease that has as primary symptoms losses of sensory and motor functions, including chronic pain. To date, however, few studies have investigated the mechanisms of chronic pain in animal models of MS since locomotor impairments render difficult its evaluation. It was previously demonstrated that in the MOG35-55-induced EAE, an animal mod...
Source: Brain, Behavior, and Immunity - Category: Neurology Source Type: research
Publication date: Available online 13 December 2019Source: Meta GeneAuthor(s): Dunya Fareed SalloomAbstractBackgroundMultiple sclerosis (MS) is a chronic neurodegenerative autoimmune disease mediated by autoreactive T cells against myelin-basic proteins. Cytokines are suggested to play a role in the etiopathogenesis of the disease. Among these cytokines is interleukin-2 (IL-2).Aim of the studyTo investigate the association between IL2+166 G/T single nucleotide polymorphism (SNP: rs2069763) and MS in Iraqi patients. Serum level of IL-2 was also detected. Anti-rubella IgG antibody was further determined in the sera of patien...
Source: Meta Gene - Category: Genetics & Stem Cells Source Type: research
Monocyte chemoattractant protein-1 (MCP-1/CCL2) is renowned for its ability to drive the chemotaxis of myeloid and lymphoid cells. It orchestrates the migration of these cell types both during physiological immune defense and in pathological circumstances, such as autoimmune diseases including rheumatoid arthritis and multiple sclerosis, inflammatory diseases including atherosclerosis, as well as infectious diseases, obesity, diabetes, and various types of cancer. However, new data suggest that the scope of CCL2's functions may extend beyond its original characterization as a chemoattractant. Emerging evidence shows that i...
Source: Frontiers in Immunology - Category: Allergy & Immunology Source Type: research
ConclusionThe downregulation in the expression of QKI-V5 in the blood of patients with CNS-inflammatory-demyelinating-diseases and in the brain and blood of EAE mice is likely caused by a circulating factor and might promote re-myelination by regulation of myelin-associated genes. Key words: QKI variants, Multiple sclerosis (MS), Neuromyelitis optica (NMO), Astrocytes, Demyelination.
Source: Multiple Sclerosis and Related Disorders - Category: Neurology Source Type: research
CONCLUSION: Our study showed decreased antioxidant capacity in newly diagnosed MS patients compared to controls. We failed to find association of subclinical atherosclerosis with oxidative stress in newly diagnosed MS. PMID: 31816220 [PubMed - as supplied by publisher]
Source: Neuroendocrinology Letters - Category: Endocrinology Tags: Neuro Endocrinol Lett Source Type: research
AbstractThe renin angiotensin system (RAS), which is classically known for blood pressure regulation, has functions beyond this. There are two axes of RAS that work to counterbalance each other and are active throughout the body, including the CNS. The pathological axis, consisting of angiotensin II (A1-8), angiotensin converting enzyme (ACE) and the angiotensin II type 1 receptor (AT1R), is upregulated in many CNS diseases, including multiple sclerosis (MS). MS is an autoimmune and neurodegenerative disease of the CNS characterized by inflammation, demyelination and axonal degeneration. Published research has described in...
Source: Journal of NeuroImmune Pharmacology - Category: Drugs & Pharmacology Source Type: research
UCLA scientists have discovered one reason why autoimmune diseases are more prevalent in women than in men. While males inherit their mother ’s X chromosome and father’s Y chromosome, females inherit X chromosomes from both parents. New research, which shows differences in how each of those X chromosomes is regulated, suggests that the X chromosome that females get from their father may help to explain their more active immune system .“It’s been known for many years that women are more susceptible to autoimmune diseases than men are,” said lead study author Dr. Rhonda Voskuhl, a UCLA professor...
Source: UCLA Newsroom: Health Sciences - Category: Universities & Medical Training Source Type: news
In conclusion, our data suggest that DKI and microstructural modeling can provide a unique contrast capable of detecting EAE-specific changes correlating with clinical disability.
Source: NeuroImage - Category: Neuroscience Source Type: research
Contributors : David Schafflick ; Maike Hartlenert ; Andreas Schulte-Mecklenbeck ; Tobias Lautwein ; Jolien Wolbert ; Gerd M HorsteSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensCerebrospinal fluid (CSF) protects the central nervous system (CNS) and analyzing CSF aids the diagnosis of CNS diseases, but our understanding of CSF leukocytes remains superficial. Here, using single cell transcriptomics, we identified a specific border-associated composition and transcriptome of CSF leukocytes. Multiple sclerosis (MS) – an autoimmune disease of the CNS – increased transcription...
Source: GEO: Gene Expression Omnibus - Category: Genetics & Stem Cells Tags: Expression profiling by high throughput sequencing Homo sapiens Source Type: research
CONCLUSIONOur findings suggest that CSF levels of the NLRP3 inflammasome may serve as a diagnostic biomarker for distinguishing NMOSD and MS. Pyroptosis mediated by the NLRP3 inflammasome following mitochondrial damage may play an important role in the pathogenesis of these neuroinflammatory disorders, especially NMOSD.Graphical abstract
Source: Multiple Sclerosis and Related Disorders - Category: Neurology Source Type: research
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