Gut human microbiota and multiple sclerosis

Kozhieva, M Kh; Melnikov, Mikhail; Rogovsky, V. S.; Oleskin, Alexander V.; Kabilov, Мarsel R.; Boyko, A. N.

doi:10.17116/jnevro201711710211-19

Cited by 17 publications

(5 citation statements)

References 86 publications

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“…Interestingly, this reduction was evident for patients with active MS, whereas patients in remission exhibited comparable diversity levels to the healthy population. Further studies verified this association of disease activity status with alterations of the relative abundance of microbes in the gut, with Firmicutes and Bacteroidetes exhibiting higher relative abundances reviewed by Kozhieva et al [61]. These studies indicated the following: Though it is widely accepted that the gut microbiome in patients with MS is characterized by moderate dysbiosis, a clear and consistent multiple sclerosis microbiome phenotype has not been described.…”

Section: Mechanisms Of Immune-modulation By Intestinal Microbiota-climentioning

confidence: 94%

Microbiome in Multiple Sclerosis: Where Are We, What We Know and Do Not Know

et al. 2020

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An increase of multiple sclerosis (MS) incidence has been reported during the last decade, and this may be connected to environmental factors. This review article aims to encapsulate the current advances targeting the study of the gut–brain axis, which mediates the communication between the central nervous system and the gut microbiome. Clinical data arising from many research studies, which have assessed the effects of administered disease-modifying treatments in MS patients to the gut microbiome, are also recapitulated.

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Section: Mechanisms Of Immune-modulation By Intestinal Microbiota-climentioning

confidence: 94%

Microbiome in Multiple Sclerosis: Where Are We, What We Know and Do Not Know

et al. 2020

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“…41,51 Moreover, insufficient exercise, obesity, gut microbiota disorders, and an "inflammatory diet" (high in meat and fat, and low in fiber and ratio of omega-3/ omega-6 fatty acids) are also known to be incentives of chronic inflammation. [52][53][54] Chronic inflammation has been linked to many chronic diseases either directly or indirectly, such as atherosclerosis, myocardial infarction, chronic heart failure, Parkinson's disease, Alzheimer's disease, asthma, diabetes, psoriasis, osteoporosis, and cancer. [55][56][57] Almost 20% of human cancers and infections have been related to chronic inflammation.…”

Section: The Initiation and Resolution Of Inflammationmentioning

confidence: 99%

Inflammation and tumor progression: signaling pathways and targeted intervention

Zhao

Yan

et al. 2021

Sig Transduct Target Ther

1,120

682

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Cancer development and its response to therapy are regulated by inflammation, which either promotes or suppresses tumor progression, potentially displaying opposing effects on therapeutic outcomes. Chronic inflammation facilitates tumor progression and treatment resistance, whereas induction of acute inflammatory reactions often stimulates the maturation of dendritic cells (DCs) and antigen presentation, leading to anti-tumor immune responses. In addition, multiple signaling pathways, such as nuclear factor kappa B (NF-kB), Janus kinase/signal transducers and activators of transcription (JAK-STAT), toll-like receptor (TLR) pathways, cGAS/STING, and mitogen-activated protein kinase (MAPK); inflammatory factors, including cytokines (e.g., interleukin (IL), interferon (IFN), and tumor necrosis factor (TNF)-α), chemokines (e.g., C-C motif chemokine ligands (CCLs) and C-X-C motif chemokine ligands (CXCLs)), growth factors (e.g., vascular endothelial growth factor (VEGF), transforming growth factor (TGF)-β), and inflammasome; as well as inflammatory metabolites including prostaglandins, leukotrienes, thromboxane, and specialized proresolving mediators (SPM), have been identified as pivotal regulators of the initiation and resolution of inflammation. Nowadays, local irradiation, recombinant cytokines, neutralizing antibodies, small-molecule inhibitors, DC vaccines, oncolytic viruses, TLR agonists, and SPM have been developed to specifically modulate inflammation in cancer therapy, with some of these factors already undergoing clinical trials. Herein, we discuss the initiation and resolution of inflammation, the crosstalk between tumor development and inflammatory processes. We also highlight potential targets for harnessing inflammation in the treatment of cancer.

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“…The involvement of dopamine in depression, cognitive impairments, and fatigue in MS was shown [ 11 , 12 , 13 , 14 ]. In addition, dopamine has been shown to modulate the gut–brain axis, which plays an important role in the development of autoimmunity, psychiatric disorders, and neuroinflammation [ 15 , 16 , 17 ]. It is important to note that depression is one of the most common symptoms in MS and may aggravate its course, which could be explained by similar pathogenetic mechanisms of MS and depression, including an enhanced Th17 immune response [ 18 , 19 ].…”

Section: The Involvement Of Dopamine In the Development Of Clinical Symptoms In Msmentioning

confidence: 99%

Dopaminergic Receptor Targeting in Multiple Sclerosis: Is There Therapeutic Potential?

Melnikov

Pashenkov

Boyко

2021

IJMS

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Dopamine is a neurotransmitter that mediates neuropsychological functions of the central nervous system (CNS). Recent studies have shown the modulatory effect of dopamine on the cells of innate and adaptive immune systems, including Th17 cells, which play a critical role in inflammatory diseases of the CNS. This article reviews the literature data on the role of dopamine in the regulation of neuroinflammation in multiple sclerosis (MS). The influence of dopaminergic receptor targeting on experimental autoimmune encephalomyelitis (EAE) and MS pathogenesis, as well as the therapeutic potential of dopaminergic drugs as add-on pathogenetic therapy of MS, is discussed.

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Gut human microbiota and multiple sclerosis

Cited by 17 publications

References 86 publications

Microbiome in Multiple Sclerosis: Where Are We, What We Know and Do Not Know

Microbiome in Multiple Sclerosis: Where Are We, What We Know and Do Not Know

Inflammation and tumor progression: signaling pathways and targeted intervention

Dopaminergic Receptor Targeting in Multiple Sclerosis: Is There Therapeutic Potential?

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