Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology最新文献

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Blocking Brain Myeloid Differentiation Factor 2-Toll-like Receptor 4 Signaling Improves Cognition by Diminishing Brain Pathologies and Preserving Adult Hippocampal Neurogenesis in Obese Rats. 阻断脑髓样分化因子2-Toll样受体4信号通过减少肥胖大鼠脑部病变和保护成年海马神经发生改善其认知能力
IF 6.2
Thura Tun Oo, Natticha Sumneang, Titikorn Chunchai, Nattayaporn Apaijai, Wasana Pratchayasakul, Guang Liang, Nipon Chattipakorn, Siriporn C Chattipakorn
{"title":"Blocking Brain Myeloid Differentiation Factor 2-Toll-like Receptor 4 Signaling Improves Cognition by Diminishing Brain Pathologies and Preserving Adult Hippocampal Neurogenesis in Obese Rats.","authors":"Thura Tun Oo, Natticha Sumneang, Titikorn Chunchai, Nattayaporn Apaijai, Wasana Pratchayasakul, Guang Liang, Nipon Chattipakorn, Siriporn C Chattipakorn","doi":"10.1007/s11481-024-10151-9","DOIUrl":"https://doi.org/10.1007/s11481-024-10151-9","url":null,"abstract":"<p><p>The myeloid differentiation factor 2 (MD-2)-toll-like receptor 4 (TLR4) signaling pathway has been linked to cognitive decline in obese rats. However, more research is required to fully understand the mechanistic role of MD-2-TLR4 signalling pathway in obese-related cognitive impairment. In this study, we used two novel MD-2 inhibitors-MAC28 (a mono-carbonyl analogue of curcumin 28) and 2i-10 (a cinnamamide-derivative compound)-to better comprehend the mechanistic role of the MD-2-TLR4 signalling pathway in obese-related cognitive impairment. A normal diet (ND) (n = 16) and a high-fat diet (HFD) (n = 64) were given to randomly divided groups of male Wistar rats for 16-weeks. At week 13, 2 types of vehicles were randomly administered to ND-fed and HFD-fed rats, whereas MAC28 (3-doses) and 2i-10 (3-doses) were randomly given to HFD-fed rats until week 16. HFD-fed rats developed obesity with metabolic disturbances, a variety of brain pathologies and cognitive decline. In obese rats, blocking the brain MD-2-TLR4 signalling pathway with MAC28 or 2i-10 improved cognition via reducing brain inflammation, neurodegeneration, microglial activation, dendritic spine loss, brain oxidative stress, as well as preserving adult hippocampal neurogenesis. Our findings highlight to better understand the role of MD-2-TLR4 signaling pathway in obese-related cognitive decline, and MD-2 could be a potential therapeutic target for brain pathologies and cognitive decline in obesity.</p>","PeriodicalId":73858,"journal":{"name":"Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology","volume":"19 1","pages":"51"},"PeriodicalIF":6.2,"publicationDate":"2024-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142382668","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Targeting Toll-like Receptor 4/Nuclear Factor-κB and Nrf2/Heme Oxygenase-1 Crosstalk via Trimetazidine Alleviates Lipopolysaccharide-Induced Depressive-like Behaviors in Mice. 通过曲美他嗪靶向 Toll-like Receptor 4/Nuclear Factor-κB 和 Nrf2/Heme Oxygenase-1 Crosstalk 减轻脂多糖诱导的小鼠抑郁样行为
IF 6.2
Sarah S Mohamed, Nora O Abdel Rasheed, Weam W Ibrahim, Nesma A Shiha
{"title":"Targeting Toll-like Receptor 4/Nuclear Factor-κB and Nrf2/Heme Oxygenase-1 Crosstalk via Trimetazidine Alleviates Lipopolysaccharide-Induced Depressive-like Behaviors in Mice.","authors":"Sarah S Mohamed, Nora O Abdel Rasheed, Weam W Ibrahim, Nesma A Shiha","doi":"10.1007/s11481-024-10149-3","DOIUrl":"10.1007/s11481-024-10149-3","url":null,"abstract":"<p><p>Depression is a global psychiatric illness that imposes a substantial economic burden. Unfortunately, traditional antidepressants induce many side effects which limit patient compliance thus, exploring alternative therapies with fewer adverse effects became urgent. This study aimed to investigate the effect of trimetazidine (TMZ); a well-known anti-ischemic drug in lipopolysaccharide (LPS) mouse model of depression focusing on its ability to regulate toll-like receptor 4 (TLR4)/nuclear factor-κB (NF-κB) as well as nuclear factor erythroid 2 related factor 2 (Nrf2)/ heme oxygenase-1 (HO-1) signaling pathways. Male Swiss albino mice were injected with LPS (500 µg/kg, i.p) every other day alone or parallel with oral doses of either escitalopram (Esc) (10 mg/kg/day) or TMZ (20 mg/kg/day) for 14 days. Treatment with TMZ attenuated LPS-induced animals' despair with reduced immobility time inforced swimming test. TMZ also diminished LPS- induced neuro-inflammation via inhibition of TLR4/NF-κB pathway contrary to Nrf2/HO-1 cascade activation with consequent increase in reduced glutathione (GSH) and HO-1 levels whereas the pro-inflammatory cytokines; tumor necrosis factor-α (TNF-α) and interleukin (IL)-1β were evidently reduced. Besides, TMZ replenished brain serotonin levels via serotonin transporter (SERT) inhibition. Thus, TMZ hindered LPS-induced neuro-inflammation, oxidative stress, serotonin deficiency besides its anti-apoptotic effect which was reflected by decreased caspase-3 level. Neuroprotective effects of TMZ were confirmed by the histological photomicrographs which showed prominent neuronal survival. Here we showed that TMZ is an affluent nominee for depression management via targeting TLR4/NF-κB and Nrf2/HO-1 pathways. Future research addressing TMZ-antidepressant activity in humans is mandatory to enroll it as a novel therapeutic strategy for depression.</p>","PeriodicalId":73858,"journal":{"name":"Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology","volume":"19 1","pages":"50"},"PeriodicalIF":6.2,"publicationDate":"2024-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11420337/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142302698","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
MFG-E8 Ameliorates Nerve Injury-Induced Neuropathic Pain by Regulating Microglial Polarization and Neuroinflammation via Integrin β3/SOCS3/STAT3 Pathway in Mice. MFG-E8通过整合素β3/SOCS3/STAT3通路调节小鼠的微胶质细胞极化和神经炎症,从而改善神经损伤诱发的神经病理性疼痛
IF 6.2
Longqing Zhang, Xinyi Dai, Danyang Li, Jiayi Wu, Shaojie Gao, Fanhe Song, Lin Liu, Yaqun Zhou, Daiqiang Liu, Wei Mei
{"title":"MFG-E8 Ameliorates Nerve Injury-Induced Neuropathic Pain by Regulating Microglial Polarization and Neuroinflammation via Integrin β3/SOCS3/STAT3 Pathway in Mice.","authors":"Longqing Zhang, Xinyi Dai, Danyang Li, Jiayi Wu, Shaojie Gao, Fanhe Song, Lin Liu, Yaqun Zhou, Daiqiang Liu, Wei Mei","doi":"10.1007/s11481-024-10150-w","DOIUrl":"10.1007/s11481-024-10150-w","url":null,"abstract":"<p><p>Spinal microglial polarization plays a crucial role in the pathological processes of neuropathic pain following peripheral nerve injury. Accumulating evidence suggests that milk fat globule epidermal growth factor-8 (MFG-E8) exhibits anti-inflammatory effect and regulates microglial polarization through the integrin β3 receptor. However, the impact of MFG-E8 on microglial polarization in the context of neuropathic pain has not yet been investigated. In this study, we evaluated the effect of MFG-E8 on pain hypersensitivity and spinal microglial polarization following spared nerve injury (SNI) of the sciatic nerve in mice. We determined the molecular mechanisms underlying the effects of MFG-E8 on pain hypersensitivity and spinal microglial polarization using pain behavior assessment, western blot (WB) analysis, immunofluorescence (IF) staining, quantitative polymerase chain reaction (qPCR), enzyme-linked immunosorbent assay (ELISA), and small interfering RNA (siRNA) transfection. Our findings indicate that SNI significantly increased the levels of MFG-E8 and integrin β3 expressed in microglia within the spinal cord of mice. Additionally, we observed that intrathecal injection of recombinant human MFG-E8 (rhMFG-E8) alleviated SNI induced-mechanical allodynia and thermal hyperalgesia. Furthermore, the results suggested that rhMFG-E8 facilitated M2 microglial polarization and ameliorated neuroinflammation via integrin β3/SOCS3/STAT3 pathway in the spinal cord of mice with SNI. Importantly, these effects were negated by integrin β3 siRNA, or SOCS3 siRNA. These results demonstrate that MFG-E8 ameliorates peripheral nerve injury induced-mechanical allodynia and thermal hyperalgesia by driving M2 microglial polarization and mitigating neuroinflammation mediated by integrin β3/SOCS3/STAT3 pathway in the spinal cord of mice. MFG-E8 may serve as a promising target for the treatment of neuropathic pain.</p>","PeriodicalId":73858,"journal":{"name":"Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology","volume":"19 1","pages":"49"},"PeriodicalIF":6.2,"publicationDate":"2024-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142302697","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Tetramerization of PKM2 Alleviates Traumatic Brain Injury by Ameliorating Mitochondrial Damage in Microglia. PKM2四聚体化通过改善小胶质细胞线粒体损伤缓解创伤性脑损伤
IF 6.2
Haiyan Zhu, Huiwen Zhang, Xiao-Jing Zhao, Lingyuan Zhang, Xue Liu, Zhi-Yuan Zhang, Yi-Zhi Ren, Yong Feng
{"title":"Tetramerization of PKM2 Alleviates Traumatic Brain Injury by Ameliorating Mitochondrial Damage in Microglia.","authors":"Haiyan Zhu, Huiwen Zhang, Xiao-Jing Zhao, Lingyuan Zhang, Xue Liu, Zhi-Yuan Zhang, Yi-Zhi Ren, Yong Feng","doi":"10.1007/s11481-024-10138-6","DOIUrl":"10.1007/s11481-024-10138-6","url":null,"abstract":"<p><p>Traumatic brain injury (TBI) is a leading cause of death and disability worldwide. Microglial activation and neuroinflammation are key cellular events that determine the outcome of TBI, especially neuronal and cognitive function. Studies have suggested that the metabolic characteristics of microglia dictate their inflammatory response. The pyruvate kinase isoform M2 (PKM2), a key glycolytic enzyme, is involved in the regulation of various cellular metabolic processes, including mitochondrial metabolism. This suggests that PKM2 may also participate in the regulation of microglial activation during TBI. Therefore, the present study aimed to evaluate the role of PKM2 in regulating microglial activation and neuroinflammation and its effects on cognitive function following TBI. A controlled cortical impact (CCI) mouse model and inflammation-induced primary mouse microglial cells in vitro were used to investigate the potential effects of PKM2 inhibition and regulation. PKM2 was significantly increased during the acute and subacute phases of TBI and was predominantly detected in microglia rather than in neurons. Our results demonstrate that shikonin and TEPP-46 can inhibit microglial inflammation, improving mitochondria, improving mouse behavior, reducing brain defect volume, and alleviating pathological changes after TBI. There is a difference in the intervention of shikonin and TEPP-46 on PKM2. Shikonin directly inhibits General PKM2; TEPP-46 can promote the expression of PKM2 tetramer. In vitro experiments, TEPP-46 can promote the expression of PKM2 tetramer, enhance the interaction between PKM2 and MFN2, improve mitochondria, alleviate neuroinflammation. General inhibition and tetramerization activation of PKM2 attenuated cognitive function caused by TBI, whereas PKM2 tetramerization exhibited a better treatment effect. Our experiments demonstrated the non-metabolic role of PKM2 in the regulation of microglial activation following TBI. Both shikonin and TEPP-46 can inhibit pro-inflammatory factors, but only TEPP-46 can promote PKM2 tetramerization and upregulate the release of anti-inflammatory factors from microglia.</p>","PeriodicalId":73858,"journal":{"name":"Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology","volume":"19 1","pages":"48"},"PeriodicalIF":6.2,"publicationDate":"2024-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142082859","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
T Cells Trafficking into the Brain in Aging and Alzheimer's Disease. 老化和阿尔茨海默病中进入大脑的 T 细胞贩运。
IF 6.2
Yue-Zhang Ma, Jia-Xin Cao, Yi-Shu Zhang, Xiao-Mei Su, Yu-Hong Jing, Li-Ping Gao
{"title":"T Cells Trafficking into the Brain in Aging and Alzheimer's Disease.","authors":"Yue-Zhang Ma, Jia-Xin Cao, Yi-Shu Zhang, Xiao-Mei Su, Yu-Hong Jing, Li-Ping Gao","doi":"10.1007/s11481-024-10147-5","DOIUrl":"https://doi.org/10.1007/s11481-024-10147-5","url":null,"abstract":"<p><p>The meninges, choroid plexus (CP) and blood-brain barrier (BBB) are recognized as important gateways for peripheral immune cell trafficking into the central nervous system (CNS). Accumulation of peripheral immune cells in brain parenchyma can be observed during aging and Alzheimer's disease (AD). However, the mechanisms by which peripheral immune cells enter the CNS through these three pathways and how they interact with resident cells within the CNS to cause brain injury are not fully understood. In this paper, we review recent research on T cells recruitment in the brain during aging and AD. This review focuses on the possible pathways through which T cells infiltrate the brain, the evidence that T cells are recruited to the brain, and how infiltrating T cells interact with the resident cells in the CNS during aging and AD. Unraveling these issues will contribute to a better understanding of the mechanisms of aging and AD from the perspective of immunity, and hopefully develop new therapeutic strategies for brain aging and AD.</p>","PeriodicalId":73858,"journal":{"name":"Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology","volume":"19 1","pages":"47"},"PeriodicalIF":6.2,"publicationDate":"2024-08-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142047567","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Sigma-1 Receptors Control Neuropathic Pain and Peripheral Neuroinflammation After Nerve Injury in Female Mice: A Transcriptomic Study. Sigma-1 受体控制雌性小鼠神经损伤后的神经性疼痛和外周神经炎症:转录组研究
IF 6.2
M Carmen Ruiz-Cantero, José M Entrena, Antonia Artacho-Cordón, Miguel Á Huerta, Enrique Portillo-Salido, Francisco R Nieto, José M Baeyens, Michael Costigan, Rafael González-Cano, Enrique J Cobos
{"title":"Sigma-1 Receptors Control Neuropathic Pain and Peripheral Neuroinflammation After Nerve Injury in Female Mice: A Transcriptomic Study.","authors":"M Carmen Ruiz-Cantero, José M Entrena, Antonia Artacho-Cordón, Miguel Á Huerta, Enrique Portillo-Salido, Francisco R Nieto, José M Baeyens, Michael Costigan, Rafael González-Cano, Enrique J Cobos","doi":"10.1007/s11481-024-10144-8","DOIUrl":"10.1007/s11481-024-10144-8","url":null,"abstract":"<p><p>The mechanisms for neuropathic pain amelioration by sigma-1 receptor inhibition are not fully understood. We studied genome-wide transcriptomic changes (RNAseq) in the dorsal root ganglia (DRG) from wild-type and sigma-1 receptor knockout mice prior to and following Spared Nerve Injury (SNI). In wildtype mice, most of the transcriptomic changes following SNI are related to the immune function or neurotransmission. Immune function transcripts contain cytokines and markers for immune cells, including macrophages/monocytes and CD4 + T cells. Many of these immune transcripts were attenuated by sigma-1 knockout in response to SNI. Consistent with this we found, using flow cytometry, that sigma-1 knockout mice showed a reduction in macrophage/monocyte recruitment as well as an absence of CD4 + T cell recruitment in the DRG after nerve injury. Sigma-1 knockout mice showed a reduction of neuropathic (mechanical and cold) allodynia and spontaneous pain-like responses (licking of the injured paw) which accompany the decreased peripheral neuroinflammatory response after nerve injury. Treatment with maraviroc (a CCR5 antagonist which preferentially inhibits CD4 + T cells in the periphery) of neuropathic wild-type mice only partially replicated the sigma-1 knockout phenotype, as it did not alter cold allodynia but attenuated spontaneous pain-like responses and mechanical hypersensitivity. Therefore, modulation of peripheral CD4 + T cell activity might contribute to the amelioration of spontaneous pain and neuropathic tactile allodynia seen in the sigma-1 receptor knockout mice, but not to the effect on cold allodynia. We conclude that sigma-1 receptor inhibition decreases DRG neuroinflammation which might partially explain its anti-neuropathic effect.</p>","PeriodicalId":73858,"journal":{"name":"Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology","volume":"19 1","pages":"46"},"PeriodicalIF":6.2,"publicationDate":"2024-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142006090","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
The Antidepressant- and Anxiolytic-Like Effects of the Phosphodiesterase Type-5 Inhibitor Tadalafil are Associated with the Modulation of the Gut-Brain Axis During CNS Autoimmunity. 5型磷酸二酯酶抑制剂他达拉非的抗抑郁和抗焦虑作用与中枢神经系统自身免疫过程中肠道-大脑轴的调节有关
IF 6.2
Eduardo Duarte-Silva, Alice Chevrollier Oriá, Ingrid Prata Mendonça, Igor Henrique Rodrigues Paiva, Klyvia Leuthier Dos Santos, Amanda Juliana Sales, José Roberto Botelho de Souza, Michael Maes, Sven Guenther Meuth, Christina Alves Peixoto
{"title":"The Antidepressant- and Anxiolytic-Like Effects of the Phosphodiesterase Type-5 Inhibitor Tadalafil are Associated with the Modulation of the Gut-Brain Axis During CNS Autoimmunity.","authors":"Eduardo Duarte-Silva, Alice Chevrollier Oriá, Ingrid Prata Mendonça, Igor Henrique Rodrigues Paiva, Klyvia Leuthier Dos Santos, Amanda Juliana Sales, José Roberto Botelho de Souza, Michael Maes, Sven Guenther Meuth, Christina Alves Peixoto","doi":"10.1007/s11481-024-10148-4","DOIUrl":"10.1007/s11481-024-10148-4","url":null,"abstract":"<p><p>Multiple Sclerosis (MS) is a debilitating disease that severely affects the central nervous system (CNS). Apart from neurological symptoms, it is also characterized by neuropsychiatric comorbidities, such as anxiety and depression. Phosphodiesterase-5 inhibitors (PDE5Is) such as Sildenafil and Tadalafil have been shown to possess antidepressant-like effects, but the mechanisms underpinning such effects are not fully characterized. To address this question, we used the EAE model of MS, behavioral tests, immunofluorescence, immunohistochemistry, western blot, and 16 S rRNA sequencing. Here, we showed that depressive-like behavior in Experimental Autoimmune Encephalomyelitis (EAE) mice is due to neuroinflammation, reduced synaptic plasticity, dysfunction in glutamatergic neurotransmission, glucocorticoid receptor (GR) resistance, increased blood-brain barrier (BBB) permeability, and immune cell infiltration to the CNS, as well as inflammation, increased intestinal permeability, and immune cell infiltration in the distal colon. Furthermore, 16 S rRNA sequencing revealed that behavioral dysfunction in EAE mice is associated with changes in the gut microbiota, such as an increased abundance of Firmicutes and Saccharibacteria and a reduction in Proteobacteria, Parabacteroides, and Desulfovibrio. Moreover, we detected an increased abundance of Erysipelotrichaceae and Desulfovibrionaceae and a reduced abundance of Lactobacillus johnsonii. Surprisingly, we showed that Tadalafil likely exerts antidepressant-like effects by targeting all aforementioned disease aspects. In conclusion, our work demonstrated that anxiety- and depressive-like behavior in EAE is associated with a plethora of neuroimmune and gut microbiota-mediated mechanisms and that Tadalafil exerts antidepressant-like effects probably by targeting these mechanisms. Harnessing the knowledge of these mechanisms of action of Tadalafil is important to pave the way for future clinical trials with depressed patients.</p>","PeriodicalId":73858,"journal":{"name":"Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology","volume":"19 1","pages":"45"},"PeriodicalIF":6.2,"publicationDate":"2024-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142001510","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Hyperalgesic Effect Evoked by il-16 and its Participation in Inflammatory Hypernociception in Mice. il-16诱发的小鼠痛觉减退效应及其在炎症性痛觉减退中的参与作用
IF 6.2
Sara González-Rodríguez, Christian Sordo-Bahamonde, Alejandro Álvarez-Artime, Ana Baamonde, Luis Menéndez
{"title":"Hyperalgesic Effect Evoked by il-16 and its Participation in Inflammatory Hypernociception in Mice.","authors":"Sara González-Rodríguez, Christian Sordo-Bahamonde, Alejandro Álvarez-Artime, Ana Baamonde, Luis Menéndez","doi":"10.1007/s11481-024-10145-7","DOIUrl":"10.1007/s11481-024-10145-7","url":null,"abstract":"<p><p>The systemic administration of interleukin-16 (IL-16, 3-30 ng/kg) induced thermal hyperalgesia in mice, that was prevented by the acute injection of an anti-CD4 antibody (1 µg/kg), the depletion of circulating white blood cells by cyclophosphamide or the specific reduction of circulating CD4<sup>+</sup> cells provoked by a high dose of an anti-CD4 antibody (30 µg/mouse, 24 h before). IL-16-induced hyperalgesia was locally inhibited after intraplantar (i.pl.) administration of the non-selective cyclooxygenase (COX) inhibitor diclofenac, the COX-1 inhibitor SC-560, the COX-2 inhibitor celecoxib, the TRPV1 antagonist capsazepine or the TRPA1 antagonist HC030031, thus demonstrating that prostaglandins and TRP channels are involved in this effect. The i.pl. administration of low doses of IL-16 (0.1-1 ng) evoked local hyperalgesia suggesting the possibility that IL-16 could participate in hypernociception associated to local tissue injury. Accordingly, IL-16 concentration measured by ELISA was increased in paws acutely inflamed with carrageenan or chronically inflamed with complete Freund´s adjuvant (CFA). This augmentation was reduced after white cell depletion with cyclophosphamide or neutrophil depletion with an anti-Ly6G antibody. Immunofluorescence and flow cytometry experiments showed that the increased concentration of IL-16 levels found in acutely inflamed paws is mainly related to the infiltration of IL-16<sup>+</sup> neutrophils, although a reduced number of IL-16<sup>+</sup> lymphocytes was also detected in paws inflamed with CFA. Supporting the functional role of IL-16 in inflammatory hypernociception, the administration of an anti-IL-16 antibody dose-dependently reduced carrageenan- and CFA-induced thermal hyperalgesia and mechanical allodynia. The interest of IL-16 as a target to counteract inflammatory pain is suggested.</p>","PeriodicalId":73858,"journal":{"name":"Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology","volume":"19 1","pages":"44"},"PeriodicalIF":6.2,"publicationDate":"2024-08-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11329551/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141997036","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Intestinal Akkermansia muciniphila is Beneficial to Functional Recovery Following Ischemic Stroke. 肠道 Akkermansia muciniphila 对缺血性中风后的功能恢复有益
IF 6.2
Kemin Li, Wancong Ding, Xinrui Li, Hao Gao, Shuang Wang, Ting Li, Haiyu Zhao, Shengxiang Zhang
{"title":"Intestinal Akkermansia muciniphila is Beneficial to Functional Recovery Following Ischemic Stroke.","authors":"Kemin Li, Wancong Ding, Xinrui Li, Hao Gao, Shuang Wang, Ting Li, Haiyu Zhao, Shengxiang Zhang","doi":"10.1007/s11481-024-10146-6","DOIUrl":"10.1007/s11481-024-10146-6","url":null,"abstract":"<p><p>Recent studies have demonstrated the interaction between gut microbiota and brain on ischemic stroke, but the roles of gut microbiota in the pathophysiology of ischemic stroke remain largely unclear. In this study, we detected a significant increase of intestinal Akkermansia muciniphila (AKK) following ischemic stroke by a rose bengal photothrombosis model. To investigate the function and mechanism of AKK on ischemic stroke, we performed the AKK administration prior to stroke surgery. The results showed that mice treated with AKK gained significantly higher body weight and behaved better than those in PBS group at 3 days after ischemic stroke. Consistently, AKK administration remarkably decreased the infarct volumes as well as the density of degenerating neurons and apoptotic cells after ischemic stroke. Notably, AKK is a potential therapeutic target in immune-related disorders connected to the microbiota, and inflammation is crucially involved in the pathophysiological process of ischemic stroke. For the determination of underlying mechanisms of this protective effect, we investigated whether there are associations between AKK and neuroinflammation following ischemic stroke. The results suggested that AKK administration significantly reduced the activation of astrocytes and microglia but up-regulated multiple anti-inflammatory factors following ischemic stroke. Therefore, our study highlighted the beneficial roles of intestinal AKK on ischemic stroke and provided a new perspective for the treatment of ischemic stroke.</p>","PeriodicalId":73858,"journal":{"name":"Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology","volume":"19 1","pages":"43"},"PeriodicalIF":6.2,"publicationDate":"2024-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141977367","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Correction: FTY720 Inhibits MPP+-Induced Microglial Activation by Affecting NLRP3 Inflammasome Activation. 更正:FTY720 通过影响 NLRP3 炎症小体的活化抑制 MPP+ 诱导的小胶质细胞活化。
IF 6.2
Shu Yao, Longjun Li, Xin Sun, Jun Hua, Keqi Zhang, Li Hao, Lixin Liu, Dongyan Shi, Hong Zhou
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