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Article ; Online: Decoding the Neurotoxic Effects of Propofol: Insights into the RARα-Snhg1-Bdnf Regulatory Cascade.

Xu, Yuhai / Xin, Xin / Tao, Tianzhu

American journal of physiology. Cell physiology

2024

Abstract: The potential neurotoxic effects of propofol, an extensively utilized anesthetic, underline the urgency to comprehend its influence on neuronal health. Insights into the role of the RARα-Snhg1-Bdnf network can offer significant advancements in minimizing ...

Abstract	The potential neurotoxic effects of propofol, an extensively utilized anesthetic, underline the urgency to comprehend its influence on neuronal health. Insights into the role of the RARα-Snhg1-Bdnf network can offer significant advancements in minimizing these effects. The study targets the exploration of the RARα and Snhg1 regulatory network's influence on Bdnf expression in the realm of propofol-induced neurotoxicity. Harnessing the GEO database and utilizing JASPAR and RPISeq for projections, the study embarks on an in-depth analysis employing both in vitro and in vivo models. The findings draw a clear link between propofol-induced neurotoxicity and the amplification of RAR signaling pathways, impacting hippocampal development and apoptosis and leading to increased RARα and Snhg1 and decreased Bdnf. Propofol is inferred to accentuate neurotoxicity by heightening RARα and Snhg1 interactions, culminating in Bdnf suppression.
Language	English
Publishing date	2024-04-15
Publishing country	United States
Document type	Journal Article
ZDB-ID	392098-7
ISSN	1522-1563 ; 0363-6143
ISSN (online)	1522-1563
ISSN	0363-6143
DOI	10.1152/ajpcell.00547.2023
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Article ; Online: Unveiling the role of PD-L1 in vascular endothelial dysfunction: Insights into the mtros/NLRP3/caspase-1 mediated pyroptotic pathway.

Tao, Tianzhu / Zhu, Ying / Shi, Yue / Sun, Bingke / Gu, Yi / Xu, Shumin

Experimental cell research

2024 Volume 438, Issue 1, Page(s) 114047

Abstract: Background: Programmed death ligand-1(PD-L1) has been postulated to play a crucial role in the regulation of barrier functions of the vascular endothelium, yet how this novel molecule mediates dysfunction in endothelial cells (ECs) during acute lung ... ...

Abstract	Background: Programmed death ligand-1(PD-L1) has been postulated to play a crucial role in the regulation of barrier functions of the vascular endothelium, yet how this novel molecule mediates dysfunction in endothelial cells (ECs) during acute lung injury (ALI) remains largely unknown. Methods: PD-L1 siRNA and plasmids were synthesized and applied respectively to down- or up-regulate PD-L1 expression in human lung microvascular endothelial cells (HMVECs). RNA sequencing was used to explore the differentially expressed genes following PD-L1 overexpression. The expression levels of tight junction proteins (ZO-1 and occludin) and the signaling pathways of NLRP-3/caspase-1/pyroptosis were analyzed. A mouse model of indirect ALI was established through hemorrhagic shock (HEM) followed by cecal ligation and puncture (CLP), enabling further investigation into the effects of intravenous delivery of PD-L1 siRNA. Results: A total of 1502 differentially expressed genes were identified, comprising 532 down-regulated and 970 up-regulated genes in ECs exhibiting PD-L1overexpression. Enrichment of PD-L1-correlated genes were observed in the NOD-like receptor signaling pathway and the TNF signaling pathway. Western blot assays confirmed that PD-L1 overexpression elevated the expression of NLRP3, cleaved-caspase-1, ASC and GSDMD, and concurrently diminished the expression of ZO-1 and occludin. This overexpression also enhanced mitochondrial oxidative phosphorylation and mitochondrial reactive oxygen species (mtROS) production. Interestingly, mitigating mitochondrial dysfunction with mitoQ partially countered the adverse effects of PD-L1 on the functionality of ECs. Furthermore, intravenous administration of PD-L1 siRNA effectively inhibited the activation of the NLRP3 inflammasome and pyroptosis in pulmonary ECs, subsequently ameliorating lung injury in HEM/CLP mice. Conclusion: PD-L1-mediated activation of the inflammasome contributes significantly to the disruption of tight junction and induction of pyroptosis in ECs, where oxidative stress associated with mitochondrial dysfunction serves as a pivotal mechanism underpinning these effects.
MeSH term(s)	Animals ; Humans ; Male ; Mice ; Acute Lung Injury/metabolism ; Acute Lung Injury/pathology ; Acute Lung Injury/genetics ; B7-H1 Antigen/metabolism ; B7-H1 Antigen/genetics ; Caspase 1/metabolism ; Caspase 1/genetics ; Endothelial Cells/metabolism ; Endothelium, Vascular/metabolism ; Endothelium, Vascular/pathology ; Mitochondria/metabolism ; NLR Family, Pyrin Domain-Containing 3 Protein/metabolism ; NLR Family, Pyrin Domain-Containing 3 Protein/genetics ; Pyroptosis/genetics ; Reactive Oxygen Species/metabolism ; Signal Transduction
Chemical Substances	B7-H1 Antigen ; Caspase 1 (EC 3.4.22.36) ; CD274 protein, human ; NLR Family, Pyrin Domain-Containing 3 Protein ; NLRP3 protein, human ; Reactive Oxygen Species ; Cd274 protein, mouse
Language	English
Publishing date	2024-04-16
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1493-x
ISSN	1090-2422 ; 0014-4827
ISSN (online)	1090-2422
ISSN	0014-4827
DOI	10.1016/j.yexcr.2024.114047
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Article: Global trends in perioperative stroke research from 2003 to 2022: a web of science-based bibliometric and visual analysis.

Ji, Shunpan / Shi, Yue / Fan, Xiaojing / Jiang, Tian / Yang, Xiaoming / Tao, Tianzhu / Ye, Bo

Frontiers in neurology

2023 Volume 14, Page(s) 1185326

Abstract: Background: Perioperative stroke is a potentially devastating complication in surgical patients, which has attracted global attention. This retrospective bibliometric and visual analysis evaluates the status and global trends in perioperative stroke ... ...

Abstract	Background: Perioperative stroke is a potentially devastating complication in surgical patients, which has attracted global attention. This retrospective bibliometric and visual analysis evaluates the status and global trends in perioperative stroke research. Methods: Papers published between 2003 and 2022 were retrieved from the Web of Science core collection. Extracted data were summarized and analyzed using Microsoft Excel and further bibliometric and co-occurrence analyses were conducted using VOSviewer and CiteSpace software. Results: Publications on perioperative stroke have increased over the years. The USA topped the list of countries with the highest number of publications and citations, while Canada had the highest mean citation frequency. The Journal of Vascular Surgery and Annals of Thoracic Surgery had the highest number of publications and citation frequency for perioperative stroke. Regarding authors, Malas, Mahmoud B. contributed the most publications to the field, and Harvard University had the highest number of publications (409 papers). Based on an overlay visualization map, timeline view, and the strongest strength burst of keywords, "antiplatelet therapy," "antithrombotic therapy," "carotid revascularization," "bleeding complications," "postoperative cognitive dysfunction," "intraoperative hypotension," "thrombectomy," "cerebral revascularization," "valve surgery," "tranexamic acid," and "frozen elephant trunk" were trending topics in perioperative stroke research. Conclusion: Publications regarding perioperative stroke have experienced rapid growth in the past 20 years and are likely to continuously increase. Research on perioperative antiplatelet and antithrombotic, cardiovascular surgery, postoperative cognitive dysfunction, thrombectomy, tranexamic acid, and frozen elephant trunk has attracted increasing attention, and these topics are emerging hotspots of present research and possible candidates for future research.
Language	English
Publishing date	2023-05-31
Publishing country	Switzerland
Document type	Systematic Review
ZDB-ID	2564214-5
ISSN	1664-2295
ISSN	1664-2295
DOI	10.3389/fneur.2023.1185326
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Article ; Online: β-patchoulene alleviates cognitive dysfunction in a mouse model of sepsis associated encephalopathy by inhibition of microglia activation through Sirt1/Nrf2 signaling pathway.

Tian, Ye / Wang, Lin / Fan, Xiaojing / Zhang, Hui / Dong, Zhiwei / Tao, Tianzhu

PloS one

2023 Volume 18, Issue 1, Page(s) e0279964

Abstract: Background: Sepsis associated encephalopathy (SAE) is a common but poorly understood complication during sepsis. Currently, there are no preventive or therapeutic agents available for this neurological disorder. The present study was designed to ... ...

Abstract	Background: Sepsis associated encephalopathy (SAE) is a common but poorly understood complication during sepsis. Currently, there are no preventive or therapeutic agents available for this neurological disorder. The present study was designed to determine the potential protective effects of β-patchoulene (β-PAE) in a mouse model of SAE and explore the putative mechanisms underpinning the beneficial effects. Materials and methods: SAE was induced in C57BL/6 mice by cecal ligation and puncture(CLP). Mice were administrated with β-PAE or saline by intra-cerebral ventricle(i.c.v) injection immediately after CLP surgery. The inhibitory avoidance tests and open field tests were performed at 24h, 48h and 7days after procedures. Cytokines expression, oxidative parameters, microglia polarization and apoptosis in the brain tissue were assessed. Sirt1, Nrf2, HO-1and cleaved-caspase3 expression in hippocampus was determined by western-blotting. Further, serum cytokines expression and spleen lymphocytes apoptosis were evaluated, and survival study was performed. Results: Septic mice suffered severe cognitive decline following CLP as evidenced by decreased memory latency time and lower frequency of line crossing in the behavioral tests. A high dose of β-PAE(1mg/kg) improved the cognitive impairment in SAE mice, which was accompanied by reduced cytokines expression and oxidative stress. Immunofluorescence assay showed that β-PAE inhibited the expression of Iba-1 and iNOS in microglia. The mechanistic study indicated that β-PAE could promote the nuclear expression of Sirt1/Nrf2 and enhance cytoplasmic HO-1 expression. Furthermore, i.c.v administration of β-PAE decreased the expression of serum cytokines and apoptosis in the spleen, thus leading to an improved 7-day survival of septic mice. Finally, blockade of Nrf2 activation with ML385 largely mitigated the protective effects of β-PAE on the cognitive function, neuroinflammation and survival in SAE mice. Conclusion: In this study, we found that β-PAE significantly altered sepsis induced neuroinflammation and microglia activation, thus reversed the cognitive decline and improved the peripheral immune function. The neuroprotective effects were possibly mediated by the activation of Sirt1/Nrf2/HO-1 pathway. β-PAE might serve as a promising therapeutic agent for SAE prevention and treatment.
MeSH term(s)	Mice ; Animals ; Sepsis-Associated Encephalopathy/drug therapy ; NF-E2-Related Factor 2/metabolism ; Neuroinflammatory Diseases ; Sirtuin 1/metabolism ; Microglia/metabolism ; Mice, Inbred C57BL ; Sepsis/complications ; Sepsis/drug therapy ; Sepsis/metabolism ; Cognitive Dysfunction/etiology ; Cognitive Dysfunction/complications ; Signal Transduction ; Cytokines/metabolism
Chemical Substances	NF-E2-Related Factor 2 ; beta-patchoulene ; Sirtuin 1 (EC 3.5.1.-) ; Cytokines ; Sirt1 protein, mouse (EC 3.5.1.-)
Language	English
Publishing date	2023-01-06
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2267670-3
ISSN	1932-6203 ; 1932-6203
ISSN (online)	1932-6203
ISSN	1932-6203
DOI	10.1371/journal.pone.0279964
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Article ; Online: β-Patchoulene Preconditioning Protects Mice Against Hepatic Ischemia-Reperfusion Injury by Regulating Nrf2/HO-1 Signaling Pathway.

Tao, Tianzhu / Ye, Bo / Xu, Yuhai / Wang, Yi / Zhu, Ying / Tian, Ye

The Journal of surgical research

2022 Volume 275, Page(s) 161–171

Abstract: Introduction: Hepatic ischemia-reperfusion (I/R) injury is one of the main causes of liver dysfunction after the liver resection and transplantation. Hepatic I/R was characterized by the tissue hypoxia during ischemia phase and oxidative stress and ... ...

Abstract	Introduction: Hepatic ischemia-reperfusion (I/R) injury is one of the main causes of liver dysfunction after the liver resection and transplantation. Hepatic I/R was characterized by the tissue hypoxia during ischemia phase and oxidative stress and immune response during hypoxia-reoxygenation. The objectives of the present study were to determine the protective effects of β-patchoulene (β-PAE), a novel bioactive agent, in a mice model of hepatic I/R injury and to explore its potential mechanisms. Methods: A segmental liver warm I/R injury model was performed by occluding the portal vessels for 1 h followed by 6-h reperfusion. Twenty-four mice were randomly divided into three groups: Sham, I/R, and I/R + β-PAE, with eight mice in each group. Mice were intravenously injected with β-PAE (10 mg/kg) or saline 2 h before surgery, and parameters were measured 6 h after designated treatment. Serum aminotransferase, histologic changes, cytokines expression, and apoptosis were determined. The potential effects of β-PAE on macrophage activation and apoptosis were further evaluated in a hypoxia and reperfusion (H/R) model in vitro. Oxidative stress markers (reactive oxygen species production and malondialdehyde) and cytokines expression were measured by commercial kits. Nrf2/HO-1 and NF-ƘB signaling pathways were determined by Western blotting. Finally, blockade of nuclear factor erythroid 2-related factor 2 (Nrf2) with ML385 was used to confirm the involvement of Nrf2/HO-1 pathway in H/R injury. Results: Hepatic I/R induced apparent tissue injury as evidenced by the increased expression of serum aminotransferase, pro-inflammatory mediators production, hepatocellular apoptosis, and necrosis. β-PAE pretreatment protected mice against I/R-induced injury, which was proved by decreased serum aminotransferase and cytokines production, reduced TUNEL-positive cells, and alleviated histopathological lesion. Immunofluorescence staining showed that β-PAE suppressed the M1 polarization of Kupffer cell induced by I/R injury. Moreover, pretreatment with β-PAE suppressed H/R-induced cytokines expression and apoptosis in cultured macrophage. The mechanistic study demonstrated that β-PAE significantly promoted the nuclear Nrf2 translocation and upregulation of HO-1 while downregulating the NF-ƘB signaling pathway in both in vivo and in vitro experiments. Furthermore, blockade of Nrf2 abolished the protective effects of β-PAE on the inhibition of H/R-mediated oxidative stress, inflammatory response, and apoptosis in vitro. Conclusions: β-PAE preconditioning protects mice against hepatic I/R, which was at least in part through the reversing disequilibrium between Nrf2/HO-1 and NF-ƘB pathways. β-PAE might serve as a promising therapeutic agent in the treatment of hepatic I/R injury.
MeSH term(s)	Animals ; Apoptosis ; Cytokines/metabolism ; Heme Oxygenase-1/metabolism ; Hypoxia ; Ischemia ; Liver Diseases/pathology ; Mice ; NF-E2-Related Factor 2/metabolism ; NF-kappa B/metabolism ; Oxidative Stress ; Reperfusion Injury/pathology ; Sesquiterpenes, Guaiane ; Signal Transduction ; Transaminases
Chemical Substances	Cytokines ; NF-E2-Related Factor 2 ; NF-kappa B ; Sesquiterpenes, Guaiane ; beta-patchoulene ; Heme Oxygenase-1 (EC 1.14.14.18) ; Transaminases (EC 2.6.1.-)
Language	English
Publishing date	2022-03-10
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80170-7
ISSN	1095-8673 ; 0022-4804
ISSN (online)	1095-8673
ISSN	0022-4804
DOI	10.1016/j.jss.2022.02.001
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Article: Global trends in research on endothelial cells and sepsis between 2002 and 2022: A systematic bibliometric analysis.

Shi, Yue / Ji, Shunpan / Xu, Yuhai / Ji, Jun / Yang, Xiaoming / Ye, Bo / Lou, Jingsheng / Tao, Tianzhu

Heliyon

2023 Volume 10, Issue 1, Page(s) e23599

Abstract: Sepsis is a systemic syndrome involving physiological, pathological, and biochemical abnormalities precipitated by infection and is a major global public health problem. Endothelial cells (ECs) dysfunction is a major contributor to sepsis-induced ... ...

Abstract	Sepsis is a systemic syndrome involving physiological, pathological, and biochemical abnormalities precipitated by infection and is a major global public health problem. Endothelial cells (ECs) dysfunction is a major contributor to sepsis-induced multiple organ failure. This bibliometric analysis aimed to identify and characterize the status, evolution of the field, and new research trends of ECs and sepsis over the past 20 years. For this analysis, the Web of Science Core Collection database was searched to identify relevant publications on ECs in sepsis published between January 1, 2002, and December 31, 2022. Microsoft Excel 2021, VOSviewer software, CiteSpace software, and the online analysis platform of literature metrology (http://bibliometric.com) were used to visualize the trends of publications' countries/regions, institutions, authors, journals, and keywords. In total, 4200 articles were identified and screened, primarily originating from 86 countries/regions and 3489 institutions. The USA was the leading contributor to this research field, providing 1501 articles (35.74 %). Harvard University's scientists were the most prolific, with 129 articles. Overall, 21,944 authors were identified, among whom Bae Jong Sup was the most prolific, contributing 129 publications. Additionally, Levi Marcel was the most frequently co-cited author, appearing 538 times. The journals that published the most articles were
Language	English
Publishing date	2023-12-12
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2835763-2
ISSN	2405-8440
ISSN	2405-8440
DOI	10.1016/j.heliyon.2023.e23599
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Article ; Online: High-Affinity Anti-VISTA Antibody Protects against Sepsis by Inhibition of T Lymphocyte Apoptosis and Suppression of the Inflammatory Response.

Tao, Tianzhu / Bo, Lulong / Li, Teng / Shi, Longbao / Zhang, Hui / Ye, Bo / Xu, Yuhai / Ma, Qingqing / Deng, Xiaoming / Zhang, Guorong

Mediators of inflammation

2021 Volume 2021, Page(s) 6650329

Abstract: Background: B7 family members and ligands have been identified as critical checkpoints in orchestrating the immune response during sepsis. V-domain Ig suppressor of T cell activation (VISTA) is a new inhibitory immune checkpoint involved in restraining ... ...

Abstract	Background: B7 family members and ligands have been identified as critical checkpoints in orchestrating the immune response during sepsis. V-domain Ig suppressor of T cell activation (VISTA) is a new inhibitory immune checkpoint involved in restraining T cell response. Previous studies demonstrated that VISTA engagement on T cells and myeloid cells could transmit inhibitory signals, resulting in reduced activation and function. The current study was designed to determine the potential therapeutic effects of a high-affinity anti-VISTA antibody (clone MH5A) in a murine model of sepsis. Methods: Polymicrobial sepsis was induced in male C57BL/6 mice via cecal ligation and puncture. Expression profiles of VISTA on T lymphocytes and macrophage were examined at 24 and 72 h postsurgery. The effects of anti-VISTA mAb on the 7-day survival, lymphocyte apoptosis, cytokine expression, bacterial burden, and vital organ damage were determined. Furthermore, the effects of anti-VISTA mAb on CD3 Results: VISTA was substantially expressed on T cells and macrophages in sham-operated mice; septic peritonitis did not induce significant changes in the expression profiles. Treatment with MH5A improved the survival of septic mice, accompanied by reduced lymphocyte apoptosis, decreased cytokine expression, and enhanced bacterial clearance. Engagement of VISTA receptor with MH5A mitigated CD3 Conclusion: The present study identified VISTA as a novel immune checkpoint in the regulation of T cell and macrophage response during sepsis. Modulation of the VISTA pathway might offer a promising opportunity in the immunotherapy for sepsis.
MeSH term(s)	Animals ; Apoptosis ; B7 Antigens/immunology ; CD3 Complex/metabolism ; Cecum ; Cytokines/metabolism ; Disease Models, Animal ; Immune System ; Immunotherapy ; Inflammation/metabolism ; Lymphocyte Activation ; Lymphocyte Count ; Macrophages/metabolism ; Male ; Membrane Proteins/metabolism ; Mice ; Mice, Inbred C57BL ; Protective Agents/pharmacology ; Sepsis/microbiology ; Sepsis/prevention & control ; Spleen/metabolism ; T-Lymphocytes/pathology ; Thymus Gland/metabolism
Chemical Substances	B7 Antigens ; CD3 Complex ; Cytokines ; Membrane Proteins ; Protective Agents ; Vsir protein, mouse
Language	English
Publishing date	2021-07-28
Publishing country	United States
Document type	Journal Article
ZDB-ID	1137605-3
ISSN	1466-1861 ; 0962-9351
ISSN (online)	1466-1861
ISSN	0962-9351
DOI	10.1155/2021/6650329
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Article: The accuracy assessment of presepsin (sCD14-ST) for mortality prediction in adult patients with sepsis and a head-to-head comparison to PCT: a meta-analysis.

Zhu, Ying / Li, Xuehui / Guo, Peiyan / Chen, Yuhan / Li, Jiandong / Tao, Tianzhu

Therapeutics and clinical risk management

2019 Volume 15, Page(s) 741–753

Abstract: Objective: ...

Abstract	Objective:
Language	English
Publishing date	2019-06-13
Publishing country	New Zealand
Document type	Journal Article
ZDB-ID	2186560-7
ISSN	1178-203X ; 1176-6336
ISSN (online)	1178-203X
ISSN	1176-6336
DOI	10.2147/TCRM.S198735
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Article ; Online: Blockade of endothelial, but not epithelial, cell expression of PD-L1 following severe shock attenuates the development of indirect acute lung injury in mice.

Xu, Shumin / Yang, Qian / Bai, Jianwen / Tao, Tianzhu / Tang, Lunxian / Chen, Yaping / Chung, Chun-Shiang / Fallon, Eleanor A / Ayala, Alfred

American journal of physiology. Lung cellular and molecular physiology

2020 Volume 318, Issue 4, Page(s) L801–L812

Abstract: This study sets out to establish the comparative contribution of PD-L1 expression by pulmonary endothelial cells (ECs) and/or epithelial cells (EpiCs) to the development of indirect acute lung injury (iALI) by taking advantage of the observation that ... ...

Abstract	This study sets out to establish the comparative contribution of PD-L1 expression by pulmonary endothelial cells (ECs) and/or epithelial cells (EpiCs) to the development of indirect acute lung injury (iALI) by taking advantage of the observation that treatment with naked siRNA by intratracheal delivery in mice primarily affects lung EpiCs, but not lung ECs, while intravenous delivery of liposomal-encapsulated siRNA largely targets vascular ECs including the lung, but not pulmonary EpiCs. We showed that using a mouse model of iALI [induced by hemorrhagic shock followed by septic challenge (Hem-CLP)], PD-L1 expression on pulmonary ECs or EpiCs was significantly upregulated in the iALI mice at 24 h post-septic insult. After documenting the selective ability of intratracheal versus intravenous delivery of PD-L1 siRNA to inhibit PD-L1 expression on EpiCs versus ECs, respectively, we observed that the iALI-induced elevation of cytokine/chemokine levels (in the bronchoalveolar lavage fluid, lung lysates, or plasma), lung myeloperoxidase and caspase-3 activities could largely only be inhibited by intravenous, but not intratracheal, delivery of PD-L1 siRNA. Moreover, intravenous, but not intratracheal, delivery led to a preservation of normal tissue architecture, lessened pulmonary edema, and reduced neutrophils influx induced by iALI. In addition, in vitro mouse endothelial cell line studies showed that PD-L1 gene knockdown by siRNA or knockout by CRISPR/Cas9-mediated gene manipulation, reduced monolayer permeability, and maintained tight junction protein levels upon recombinant IFN-γ stimulation. Together, these data imply a critical role for pulmonary vascular ECs in mediating PD-1:PD-L1-driven pathological changes resulting from systemic stimuli such as Hem-CLP.
MeSH term(s)	Acute Lung Injury/metabolism ; Animals ; B7-H1 Antigen/metabolism ; Bronchoalveolar Lavage Fluid ; Cells, Cultured ; Chemokines/metabolism ; Cytokines/metabolism ; Disease Models, Animal ; Endothelial Cells/metabolism ; Epithelial Cells/metabolism ; Lung/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Neutrophils/metabolism ; Peroxidase/metabolism ; RNA, Small Interfering/metabolism ; Sepsis/metabolism ; Shock, Hemorrhagic/metabolism
Chemical Substances	B7-H1 Antigen ; Cd274 protein, mouse ; Chemokines ; Cytokines ; RNA, Small Interfering ; Peroxidase (EC 1.11.1.7)
Language	English
Publishing date	2020-01-29
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1013184-x
ISSN	1522-1504 ; 1040-0605
ISSN (online)	1522-1504
ISSN	1040-0605
DOI	10.1152/ajplung.00108.2019
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Zs.A 2749: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)

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Article ; Online: Blockade of IL-17A/IL-17R Pathway Protected Mice from Sepsis-Associated Encephalopathy by Inhibition of Microglia Activation.

Ye, Bo / Tao, Tianzhu / Zhao, Andong / Wen, Liyuan / He, Xiaofei / Liu, Yi / Fu, Qiang / Mi, Weidong / Lou, Jingsheng

Mediators of inflammation

2019 Volume 2019, Page(s) 8461725

Abstract: Sepsis-associated encephalopathy (SAE) is a poorly understood condition that leads to long-term cognitive impairment and increased mortality in survivors. Recent research revealed that IL-17A/IL-17R might serve as a checkpoint in microglia-mediated ... ...

Abstract	Sepsis-associated encephalopathy (SAE) is a poorly understood condition that leads to long-term cognitive impairment and increased mortality in survivors. Recent research revealed that IL-17A/IL-17R might serve as a checkpoint in microglia-mediated neuroinflammation. The present study was designed to determine the specific role of IL-17A-mediated microglia activation in the development of SAE. A mouse model of SAE was induced by cecal ligation and puncture (CLP), and behavior performance was evaluated by the inhibitory avoidance test and the open field test. Cytokine expression and microglia activation in brain tissue were determined at 6 h, 12 h, 24 h, 48 h, and day 7 post surgery. Further, septic mice were intracerebral ventricle- (i.c.v.-) injected with recombinant IL-17A, anti-IL-17A ab, anti-IL-17R ab, or isotype controls to evaluate the potential effects of IL-17A/IL-17R blockade in the prevention of SAE. Septic peritonitis induced significant impairment of learning memory and exploratory activity, which was associated with a higher expression of IL-17A, IL-1
MeSH term(s)	Animals ; Antibodies/therapeutic use ; Brain/drug effects ; Brain/metabolism ; Cells, Cultured ; Cognitive Dysfunction/physiopathology ; Disease Models, Animal ; Fluorescent Antibody Technique ; Interleukin-17/antagonists & inhibitors ; Interleukin-17/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Microglia/drug effects ; Microglia/metabolism ; Receptors, Interleukin-17/antagonists & inhibitors ; Receptors, Interleukin-17/metabolism ; Sepsis-Associated Encephalopathy/metabolism ; Signal Transduction/drug effects
Chemical Substances	Antibodies ; IL17A protein, human ; Il17ra protein, mouse ; Interleukin-17 ; Receptors, Interleukin-17
Language	English
Publishing date	2019-10-07
Publishing country	United States
Document type	Journal Article
ZDB-ID	1137605-3
ISSN	1466-1861 ; 0962-9351
ISSN (online)	1466-1861
ISSN	0962-9351
DOI	10.1155/2019/8461725
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Jg. 1995 - 2021: Lesesall (2.OG)
ab Jg. 2022: Lesesaal (EG)

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