Brain-gut axis dysfunction in the pathogenesis of traumatic brain injury DOI Open Access
Marie Hanscom, David J. Loane, Terez Shea‐Donohue

et al.

Journal of Clinical Investigation, Journal Year: 2021, Volume and Issue: 131(12)

Published: June 14, 2021

Traumatic brain injury (TBI) is a chronic and progressive disease, management requires an understanding of both the primary neurological secondary sequelae that affect peripheral organs, including gastrointestinal (GI) tract. The brain-gut axis composed bidirectional pathways through which TBI-induced neuroinflammation neurodegeneration impact gut function. resulting dysautonomia systemic inflammation contribute to GI events, dysmotility increased mucosal permeability. These effects shape, are shaped by, changes in microbiota composition activation resident recruited immune cells. Microbial products cell mediators turn modulate activity. Importantly, enteric inflammatory challenges prolong worsen neuropathology neurobehavioral deficits. importance communication maintaining homeostasis highlights it as viable therapeutic target for TBI. Currently, treatments directed toward dysautonomia, dysbiosis, and/or offer most promise.

Language: Английский

Gut Microbial Dysbiosis in the Pathogenesis of Gastrointestinal Dysmotility and Metabolic Disorders DOI Open Access
Rajan Singh, Hannah Zogg, Lai Wei

et al.

Journal of Neurogastroenterology and Motility, Journal Year: 2020, Volume and Issue: 27(1), P. 19 - 34

Published: Nov. 9, 2020

Of all microorganisms in the human body, largest and most complex population resides gastrointestinal (GI) tract. The gut microbiota continuously adapts to host environment serves multiple critical functions for their hosts, including regulating immunity, procuring energy from food, preventing colonization of pathogens. Mounting evidence has suggested microbial imbalance (dysbiosis) as a core pathophysiology development GI motility metabolic disorders, such irritable bowel syndrome diabetes. Current research focused on discovering associations between these disorders dysbiosis; however, whether are consequence or cause is still mostly unexplored. State-of-the-art studies have investigated how microbes communicate with our body systems through microbiota-derived metabolites they able modulate physiology. There now mounting that alterations composition small intestinal an association dysmotility disorders. Although treatment options dysbiosis currently limited, antibiotics, fecal transplantation, probiotics, dietary interventions best options. However, broad-spectrum antibiotics been viewed skepticism due risk developing antibiotic resistant bacteria. Studies warranted elucidate cellular molecular pathways underlying microbiota-host crosstalk powerful platform future therapeutic approaches. Here, we review recent literature and/or interactions involved

Language: Английский

Citations

185

Gut Microbiota in Alzheimer’s Disease, Depression, and Type 2 Diabetes Mellitus: The Role of Oxidative Stress DOI Creative Commons
Maria Luca, M. Di Mauro, Marco Di Mauro

et al.

Oxidative Medicine and Cellular Longevity, Journal Year: 2019, Volume and Issue: 2019, P. 1 - 10

Published: April 17, 2019

Gut microbiota consists of over 100 trillion microorganisms including at least 1000 different species bacteria and is crucially involved in physiological pathophysiological processes occurring the host. An imbalanced gastrointestinal ecosystem (dysbiosis) seems to be a contributor development maintenance several diseases, such as Alzheimer’s disease, depression, type 2 diabetes mellitus. Interestingly, three disorders are frequently associated demonstrated by high comorbidity rates. In this review, we introduce gut its role both normal pathological processes; then, discuss importance gut-brain axis well oxidative stress inflammation mediators which dysbiosis involved. Specific sections pertain altered pathogenesis The therapeutic implications manipulation briefly discussed. Finally, conclusion comments on possible common pathogenetic (via inflammation) shared disorders.

Language: Английский

Citations

174

Emerging role of gut microbiota in modulation of neuroinflammation and neurodegeneration with emphasis on Alzheimer's disease DOI

Divya Goyal,

Syed Afroz Ali,

Rakesh Kumar Singh

et al.

Progress in Neuro-Psychopharmacology and Biological Psychiatry, Journal Year: 2020, Volume and Issue: 106, P. 110112 - 110112

Published: Sept. 16, 2020

Language: Английский

Citations

165

Detrimental and protective action of microglial extracellular vesicles on myelin lesions: astrocyte involvement in remyelination failure DOI Creative Commons
Marta Lombardi, Roberta Parolisi, Federica Scaroni

et al.

Acta Neuropathologica, Journal Year: 2019, Volume and Issue: 138(6), P. 987 - 1012

Published: July 30, 2019

Microglia are highly plastic immune cells which exist in a continuum of activation states. By shaping the function oligodendrocyte precursor (OPCs), brain differentiate to myelin-forming cells, microglia participate both myelin injury and remyelination during multiple sclerosis. However, mode(s) action supporting or inhibiting repair is still largely unclear. Here, we analysed effects extracellular vesicles (EVs) produced vitro by either pro-inflammatory pro-regenerative on OPCs at demyelinated lesions caused lysolecithin injection mouse corpus callosum. Immunolabelling for proteins electron microscopy showed that EVs released blocked remyelination, whereas co-cultured with immunosuppressive mesenchymal stem promoted OPC recruitment repair. The molecular mechanisms responsible harmful beneficial EV actions were dissected primary cultures. exposing OPCs, cultured alone astrocytes, inflammatory EVs, observed blockade maturation only presence implicating these failure. Biochemical fractionation revealed astrocytes may be converted into cargo, as indicated immunohistochemical qPCR analyses, surface lipid components promote migration and/or differentiation, linking lipids Although through species enhance remain fully defined, provide first demonstration vesicular sphingosine 1 phosphate stimulates migration, fundamental step From this study, microglial emerge multimodal multitarget signalling mediators able influence around lesions, exploited develop novel approaches not sclerosis, but also neurological neuropsychiatric diseases characterized demyelination.

Language: Английский

Citations

152

Brain-gut axis dysfunction in the pathogenesis of traumatic brain injury DOI Open Access
Marie Hanscom, David J. Loane, Terez Shea‐Donohue

et al.

Journal of Clinical Investigation, Journal Year: 2021, Volume and Issue: 131(12)

Published: June 14, 2021

Traumatic brain injury (TBI) is a chronic and progressive disease, management requires an understanding of both the primary neurological secondary sequelae that affect peripheral organs, including gastrointestinal (GI) tract. The brain-gut axis composed bidirectional pathways through which TBI-induced neuroinflammation neurodegeneration impact gut function. resulting dysautonomia systemic inflammation contribute to GI events, dysmotility increased mucosal permeability. These effects shape, are shaped by, changes in microbiota composition activation resident recruited immune cells. Microbial products cell mediators turn modulate activity. Importantly, enteric inflammatory challenges prolong worsen neuropathology neurobehavioral deficits. importance communication maintaining homeostasis highlights it as viable therapeutic target for TBI. Currently, treatments directed toward dysautonomia, dysbiosis, and/or offer most promise.

Language: Английский

Citations

152