Neurochemical effects of sepsis on the brain DOI
Tatiana Barichello, Vijayasree V. Giridharan, Carlos Henrique Rocha Catalão

et al.

Clinical Science, Journal Year: 2023, Volume and Issue: 137(6), P. 401 - 414

Published: March 1, 2023

Sepsis is a life-threatening organ dysfunction triggered by dysregulated host immune response to eliminate an infection. After the activated, complex, dynamic, and time-dependent process triggered. This promotes production of inflammatory mediators, including acute-phase proteins, complement system cytokines, chemokines, antimicrobial peptides, which are required initiate environment for eliminating invading pathogen. The physiological this sepsis-induced systemic inflammation can affect blood-brain barrier (BBB) function; subsequently, endothelial cells produce matrix metalloproteinases (MMPs) that degrade tight junction (TJ) proteins decrease BBB function. resulting permeability allows peripheral from bloodstream enter brain, then release range mediators activate glial cells. activated microglia astrocytes reactive oxygen species (ROS), neurochemicals, mitochondrial neuronal damage, exacerbate milieu in brain. These changes trigger sepsis-associated encephalopathy (SAE), has potential increase cognitive deterioration susceptibility decline later life.

Language: Английский

Neurological manifestations associated with SARS-CoV-2 and other coronaviruses: A narrative review for clinicians DOI Open Access
A. Maury, Aïcha Lyoubi, Nathan Peiffer‐Smadja

et al.

Revue Neurologique, Journal Year: 2020, Volume and Issue: 177(1-2), P. 51 - 64

Published: Dec. 16, 2020

Language: Английский

Citations

217
Sepsis-Associated Encephalopathy and Blood-Brain Barrier Dysfunction DOI
Qingzeng Gao, Marina S. Hernandes

Inflammation, Journal Year: 2021, Volume and Issue: 44(6), P. 2143 - 2150

Published: July 21, 2021

Language: Английский

Citations

136
Sepsis-associated brain injury: underlying mechanisms and potential therapeutic strategies for acute and long-term cognitive impairments DOI Creative Commons
Nobufumi Sekino, Magdy Selim, Amjad Shehadah

et al.

Journal of Neuroinflammation, Journal Year: 2022, Volume and Issue: 19(1)

Published: April 29, 2022

Abstract Sepsis is a life-threatening organ dysfunction caused by dysregulated host response to infection. causes cerebral in the short and long term induces disruption of blood–brain barrier (BBB), neuroinflammation, hypoperfusion, accumulation amyloid β (Aβ) tau protein brain. White matter changes brain atrophy can be detected using imaging, but unfortunately, there no specific treatment that directly addresses underlying mechanisms cognitive impairments sepsis. Here, we review sepsis-associated injury, with focus on BBB Aβ We also describe neurological manifestations imaging findings finally, propose potential therapeutic strategies for acute long-term associated In phase sepsis, suggest antibiotics (such as rifampicin), targeting proinflammatory cytokines, preventing ischemic injuries hypoperfusion. late dysfunction, phosphorylation, glycogen synthase kinase-3 beta (GSK3β), receptor advanced glycation end products (RAGE). These proposed are meant bring new mechanism-based directions future basic clinical research aimed at or ameliorating patients

Language: Английский

Citations

83
β-Nicotinamide mononucleotide activates NAD+/SIRT1 pathway and attenuates inflammatory and oxidative responses in the hippocampus regions of septic mice DOI Creative Commons

Hui-ru Li,

Qiang Liu, Cheng‐long Zhu

et al.

Redox Biology, Journal Year: 2023, Volume and Issue: 63, P. 102745 - 102745

Published: May 13, 2023

Sepsis-associated encephalopathy (SAE) is one of the common serious complications in sepsis, and pathogenesis SAE remains unclear. Sirtuin 1 (SIRT1) has been reported to be downregulated hippocampus SIRT1 agonists can attenuated cognitive dysfunction septic mice. Nicotinamide adenine dinucleotide (NAD+) a key substrate maintain deacetylation activity SIRT1. As an intermediate NAD+, β-Nicotinamide Mononucleotide (NMN) promising treating neurodegenerative diseases cerebral ischemic injury. Thus we sought investigate potential role NMN treatment. The model was established by cecal ligation puncture (CLP) vivo, neuroinflammation with LPS-treated BV-2 cells vitro. Memory impairment assessed Morris water maze fear conditioning tests. result, levels PGC-1α were significantly reduced mice, while acetylation total lysine, phosphorylation P38 P65 enhanced. All these changes induced sepsis inverted NMN. Treating resulted improved behavior performance tests maze. Apoptosis, inflammatory oxidative responses mice after administration. These protective effect against memory dysfunction, injuries reversed inhibitor, EX-527. Similarly, LPS-induced activation NMN, EX-527 or knockdown could reverse such In conclusion, sepsis-induced region NAD+/SIRT1 pathway might involved mechanisms effect.

Language: Английский

Citations

56
Neurologic manifestations associated with COVID-19: a multicentre registry DOI Creative Commons
Elodie Meppiel, Nathan Peiffer‐Smadja,

Alexandra Maury

et al.

Clinical Microbiology and Infection, Journal Year: 2020, Volume and Issue: 27(3), P. 458 - 466

Published: Nov. 13, 2020

Language: Английский

Citations

134
Orbitofrontal involvement in a neuroCOVID‐19 patient DOI Open Access
Loïc Le Guennec,

Julia Devianne,

Laurence Jalin

et al.

Epilepsia, Journal Year: 2020, Volume and Issue: 61(8)

Published: June 27, 2020

Neurological manifestations of coronavirus disease 19 (COVID-19) such as encephalitis and seizures have been reported increasingly, but our understanding COVID-19-related brain injury is still limited. Herein we describe prefrontal involvement in a patient with COVID-19 who presented prior anosmia, raising the question potential trans-olfactory bulb invasion.

Language: Английский

Citations

84
Fecal Microbiota Transplantation: A New Therapeutic Attempt from the Gut to the Brain DOI Creative Commons
Haoming Xu,

Hong‐Li Huang,

Youlian Zhou

et al.

Gastroenterology Research and Practice, Journal Year: 2021, Volume and Issue: 2021, P. 1 - 20

Published: Jan. 16, 2021

Gut dysbacteriosis is closely related to various intestinal and extraintestinal diseases. Fecal microbiota transplantation (FMT) a biological therapy that entails transferring the gut from healthy individuals patients in order reconstruct microflora latter. It has been proved be an effective treatment for recurrent Clostridium difficile infection. Studies show plays important role pathophysiology of neurological psychiatric disorders through microbiota-gut-brain axis. Therefore, reconstruction promising new strategy treating cerebral We have reviewed latest research on different nervous system diseases as well FMT context its application neurological, psychiatric, other system-related (Parkinson's disease, Alzheimer's multiple sclerosis, epilepsy, autism spectrum disorder, bipolar hepatic encephalopathy, neuropathic pain, etc.).

Language: Английский

Citations

78
Brain injury in COVID-19 is associated with dysregulated innate and adaptive immune responses DOI Creative Commons
Edward Needham, Alexander Ren, Richard Digby

et al.

Brain, Journal Year: 2022, Volume and Issue: 145(11), P. 4097 - 4107

Published: Sept. 6, 2022

COVID-19 is associated with neurological complications including stroke, delirium and encephalitis. Furthermore, a post-viral syndrome dominated by neuropsychiatric symptoms common, seemingly unrelated to severity. The true frequency underlying mechanisms of injury are unknown, but exaggerated host inflammatory responses appear be key driver We investigated the dynamics of, relationship between, serum markers brain [neurofilament light (NfL), glial fibrillary acidic protein (GFAP) total tau] dysregulated response (autoantibody production cytokine profiles) in 175 patients admitted 45 influenza. During hospitalization, sera from demonstrated elevations NfL GFAP severity-dependent manner, evidence ongoing active at follow-up 4 months later. These biomarkers were pro-inflammatory cytokines presence autoantibodies large number different antigens. Autoantibodies commonly seen against lung surfactant proteins also such as myelin glycoprotein. Commensurate findings influenza cohort. A distinct process characterized elevation tau was follow-up, which appeared independent initial disease severity not immune unlike GFAP. results demonstrate that common consequence both influenza, therefore likely feature severe viral infection more broadly. occurs context dysregulation innate adaptive responses, no single pathogenic mechanism clearly responsible.

Language: Английский

Citations

66
Central role of microglia in sepsis-associated encephalopathy: From mechanism to therapy DOI Creative Commons
Xiaoqian Yan, Kaiying Yang, Qi Xiao

et al.

Frontiers in Immunology, Journal Year: 2022, Volume and Issue: 13

Published: July 26, 2022

Sepsis-associated encephalopathy (SAE) is a cognitive impairment associated with sepsis that occurs in the absence of direct infection central nervous system or structural brain damage. Microglia are thought to be macrophages system, devouring bits neuronal cells and dead brain. They activated various ways, microglia-mediated neuroinflammation characteristic diseases, including SAE. Here, we systematically described pathogenesis SAE demonstrated microglia closely related occurrence development Furthermore, comprehensively discussed function phenotype summarized their activation mechanism role pathogenesis. Finally, this review summarizes recent studies on treating by blocking microglial toxic factors produced after activation. We suggest targeting may putative treatment for

Language: Английский

Citations

61
Neuroinflammation in Sepsis: Molecular Pathways of Microglia Activation DOI Creative Commons
Carolina A. Moraes, Camila Zaverucha-do-Valle, Renaud Fleurance

et al.

Pharmaceuticals, Journal Year: 2021, Volume and Issue: 14(5), P. 416 - 416

Published: May 1, 2021

Frequently underestimated, encephalopathy or delirium are common neurological manifestations associated with sepsis. Brain dysfunction occurs in up to 80% of cases and is directly increased mortality long-term neurocognitive consequences. Although the central nervous system (CNS) has been classically viewed as an immune-privileged system, neuroinflammation emerging a mechanism brain Microglial cells major players this setting. Here, we aimed discuss current knowledge on how affected by peripheral immune activation sepsis role microglia these processes. This review focused molecular pathways microglial activity sepsis, its regulatory mechanisms, their interaction other CNS cells, especially neuronal circuits.

Language: Английский

Citations

59