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TPOL triggers apoptosis with mitochondrial injury through activating a ROS-dependent p53/p21/p27/Rb/Bax/Cyto C/caspase-mediated signaling

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中国病理生理杂志 2024年第8期40卷 1488-1496页

作者： CHENG Zongwei ZENG Boning XING Feiyue Department of immunobiology Institute of Tissue Transplantation and ImmunologyJinan UniversityGuangzhou 510632China

AIM:To explore the influence of ethyl(2,4,6-trimethylbenzoyl)phenylphosphinate(TPOL)on cell apoptosis and its potential ***:HEK293T cells sensitive to TPOL were treated with different concentrations of TPOL with or without exposure to light radiation,before treatment with various inhibitors,N-acetyl-Lcysteine(NAC),pifithrin-αand *** viability was measured by CCK-8 *** V/propidium iodide staining was used to count the number of apoptotic ***-DA staining was used to detect reactive oxygen species(ROS)levels,and JC-1 staining was used to assess mitochondrial membrane potential by flow *** expression of apoptosis-related proteins and cell cycle-regulated molecules was measured by Western ***:TPOL enhanced the apoptosis of HEK293T cells in a dose-dependent manner(P<0.05),with a decrease in Bcl-2 and increases in Bax and cytochrome C(Cyto C),followed by up-regulation of activated caspase-9 and caspase-3,and the cleavage of PARP(P<0.05).The TPOL-enhanced cleavage of caspase-3 and PARP was rescued by Z-DVED-FMK(P<0.01).TPOL also led to a rapid increase in ROS,a reduction in mitochondrial membrane potential,and the release of Cyto C(P<0.01),all of which could be reversed by the ROS scavenger ***,the TPOL-caused alterations in p21,p27,Rb,and CDK2 were also recovered by the p53 inhibitor pifithrin-α(P<0.05).The TPOL-induced changes in Bax,Bcl-2,cleaved caspase-9,activated caspase-3,and cleaved PARP were subsequently rescued by pretreatment with pifithrin-α(P<0.05).CONCLUSION:TPOL can induce cellular apoptosis with ROS-mediated mitochondrial membrane damage through the activation of a ROS-dependent p53/p21/p27/Rb/Bax/Cyto C/caspase-mediated signal axis.

关键词： ethyl(2,4,6-trimethylbenzoyl)phenylphosphinate reactive oxygen species mitochondria apoptosis

Aging-induced memory loss due to decreased N1-acetyl-5-methoxykynuramine,a melatonin metabolite,in the hippocampus:a potential prophylactic agent for dementia

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Neural Regeneration Research 2025年第6期20卷 1705-1706页

作者： Kazuki Watanabe Atsuhiko Hattori Department of immunobiology Institute of Development Aging and CancerTohoku UniversitySendaiMiyagiJapan Department of Sport and Wellness College of Sport and WellnessRikkyo UniversityNiizaSaitamaJapan

Melatonin(N-acetyl-5-methoxytryptamine)is known as the hormone of darkness because it is synthesized at night and involved in regulating the circadian *** hormone is primarily synthesized by the vertebrate pineal gland,but is ubiquitous among invertebrates,unicellular organisms,plants,and even cyanobacteria(Hattori and Suzuki,2024).Melatonin is well-conserved evolutionarily and possesses several physiological functions,such as immune response,bone and glucose metabolism,and memory formation besides regulating the circadian rhythm.

关键词： metabolism primarily agent

COVID-19 vaccination produces exercise-responsive SARS-CoV-2 specific T-cells regardless of infection history

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Journal of Sport and Health Science 2024年第1期13卷 99-107页

作者： Kyle A.Smith Tiffany M.Zúñiga Forrest L.Baker Helena Batatinha Charles R.Pedlar Shane C.Burgess Michael P.Gustafson Emmanuel Katsanis Richard J.Simpson School of Nutritional Sciences and Wellness The University of ArizonaTucsonAZ 85721USA Department of Pediatrics The University of ArizonaTucsonAZ 85724USA Faculty of Sport Allied Health and Performance ScienceSt.Mary's UniversityTwickenham TW14SXUK Institute of Sport Exercise and Health University College LondonLondon WC1E 7HUUK Department of Animal and Comparative Biomedical Sciences The University of ArizonaTucsonAZ 85721USA The University of Arizona Cancer Center The University of ArizonaTucsonAZ 85719USA Laboratory Medicine and Pathology Mayo Clinic ArizonaPhoenixAZ 85054USA Department of immunobiology The University of ArizonaTucsonAZ 85724USA Department of Medicine The University of ArizonaTucsonAZ 85724USA Department of Pathology The University of ArizonaTucsonAZ 85724USA

Background:The mobilization and redistribution of severe acute respiratory syndrome coronavirus 2(SARS-CoV-2)specific T-cells and neutralizing antibodies(nAbs)during exercise is purported to increase immune surveillance and protect against severe coronavirus disease 2019(COVID-19).We sought to determine if COVID-19 vaccination would elicit exercise-responsive SARS-CoV-2 T-cells and transiently alter nAb ***:Eighteen healthy participants completed a 20-min bout of graded cycling exercise before and/or after receiving a COVID-19 *** major leukocyte subtypes were enumerated before,during,and after exercise by flow cytometry,and immune responses to SARS-CoV-2 were determined using whole blood peptide stimulation assays,T-cell receptor(TCR)-βsequencing,and SARS-CoV-2 nAb ***:COVID-19 vaccination had no effect on the mobilization or egress of major leukocyte subsets in response to intensity-controlled graded ***,non-infected participants had a significantly reduced mobilization of CD4+and CD8+naive T-cells,as well as CD4+central memory T-cells,after vaccination(synthetic immunity group);this was not seen after vaccination in those with prior SARS-CoV-2 infection(hybrid immunity group).Acute exercise after vaccination robustly mobilized SARS-CoV-2 specific T-cells to blood in an intensity-dependent *** groups mobilized T-cells that reacted to spike protein;however,only the hybrid immunity group mobilized T-cells that reacted to membrane and nucleocapsid *** increased significantly during exercise only in the hybrid immunity ***:These data indicate that acute exercise mobilizes SARS-CoV-2 specific T-cells that recognize spike protein and increases the redistribution of nAbs in individuals with hybrid immunity.

关键词： Anti-viral COVID-19 Exercise immunology SARS-CoV-2 T-Cells Vaccine

Metabolism of tissue macrophages in homeostasis and pathology

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Cellular & Molecular Immunology 2022年第3期19卷 384-408页

作者： Stefanie K.Wculek Gillian Dunphy Ignacio Heras-Murillo Annalaura Mastrangelo David Sancho immunobiology Laboratory Centro Nacional de Investigaciones Cardiovasculares(CNIC)Melchor Fernández Almagro 3Madrid28029Spain

Cellular metabolism orchestrates the intricate use of tissue fuels for catabolism and anabolism to generate cellular energy and structural *** emerging field of immunometabolism highlights the importance of cellular metabolism for the maintenance and activities of immune *** are embryo-or adult bone marrow-derived leukocytes that are key for healthy tissue homeostasis but can also contribute to pathologies such as metabolic syndrome,atherosclerosis,fibrosis or *** metabolism has largely been studied in ***,different organs contain diverse macrophage populations that specialize in distinct and often tissue-specific *** context specificity creates diverging metabolic challenges for tissue macrophage populations to fulfill their homeostatic roles in their particular microenvironment and conditions their response in pathological ***,we outline current knowledge on the metabolic requirements and adaptations of macrophages located in tissues during homeostasis and selected diseases.

关键词： Tissue macrophages metabolism homeostasis pathology tissue regeneration

Microenvironmental influences on T cell immunity in cancer and inflammation

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Cellular & Molecular Immunology 2022年第3期19卷 316-326页

作者： Darren R.Heintzman Emilie L.Fisher Jeffrey C.Rathmell Department of Pathology Microbiologyand ImmunologyVanderbilt University Medical CenterNashvilleTN37205USA Vanderbilt Center for immunobiology Vanderbilt University Medical CenterNashvilleTN37205USA

T cell metabolism is dynamic and highly *** the intrinsic metabolic programs of T cell subsets are integral to their distinct differentiation and functional patterns,the ability of cells to acquire nutrients and cope with hostile microenvironments can limit these pathways.T cells must function in a wide variety of tissue settings,and how T cells interpret these signals to maintain an appropriate metabolic program for their demands or if metabolic mechanisms of immune suppression restrain immunity is an area of growing *** in inflamed and cancer tissues,a wide range of changes in physical conditions and nutrient availability are now acknowledged to shape *** include fever and increased temperatures,depletion of critical micro and macro-nutrients,and accumulation of inhibitory waste *** we review several of these factors and how the tissue microenvironment both shapes and constrains immunity.

关键词： immunometabolism T cell microenvironment cancer inflammation

D-半乳糖葡胺增敏小鼠对非致死剂量细菌脂多糖致死作用与肝脏DNA片段化的高度相关性(英文)

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Acta Pharmacologica Sinica 2003年第3期24卷 3-8页

作者：周炳荣 ,Marina GUMENSCHEIMER,Marina FREUDENBERG,Chris GALANOS Max-Planck-Institute for immunobiology Stiibeweg 51 D-79108 Freiburg i Br Germany Max-Planck-Institute for immunobiology Stiibeweg 51 D-79108 Freiburg i Br Germany Max-Planck-Institute for immunobiology Stiibeweg 51 D-79108 Freiburg i Br Germany

目的:本实验研究了以非致死剂量脂多糖(Lipopolysaccharide,LPS)攻击半乳糖葡胺(D-galactosamine,D-GalN)增敏小鼠的死亡是否伴有重要器官的凋亡特征。方法:实验组小鼠以LPS(0.05μg)与D-GalN(20mg)直接攻击,而对照组小鼠仅仅以LPS或D-G... 详细信息

目的:本实验研究了以非致死剂量脂多糖(Lipopolysaccharide,LPS)攻击半乳糖葡胺(D-galactosamine,D-GalN)增敏小鼠的死亡是否伴有重要器官的凋亡特征。方法:实验组小鼠以LPS(0.05μg)与D-GalN(20mg)直接攻击,而对照组小鼠仅仅以LPS或D-GalN,在规定实验时间经乙醚麻醉后,取出脑、肾、心、脾、肺、肝,并立即匀浆和抽提DNA,对所抽提的各器官的DNA以常规琼脂糖凝胶电泳分析是否存在DNA梯度现象;并测定血浆中乳酸脱氢酶和谷氨酸草酰乙酸转移酶,同时将DNA片段化现象与小鼠致死作用的关联性在实验组和对照组间做比较。结果:LPS攻击B-GalN增敏的小鼠4h时,在所检测的器官中,仅仅肝脏可见到凋亡特征DNA片段化现象,至7h时小鼠死亡。而仅用LPS或D-GalN攻击的对照组小鼠,不仅全部存活而且肝脏DNA分子完整。结论:LPS攻击B-GalN增敏的小鼠,肝脏是唯一出现DNA片段化的靶器官,由细菌LPS引发小鼠的死亡,肝脏的损伤可能是关键的原因。

关键词：脂多糖类 D-半乳糖葡胺细胞凋亡 DNA断片

The RNA helicase DHX15 is a critical regulator of natural killer-cell homeostasis and functions

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Cellular & Molecular Immunology 2022年第6期19卷 687-701页

作者： Guangchuan Wang Xiang Xiao Yixuan Wang Xiufeng Chu Yaling Dou Laurie J.Minze Rafik M.Ghobrial Zhiqiang Zhang Xian C.Li immunobiology and Transplant Science Center and Department of Surgery Houston Methodist HospitalTexas Medical CenterHoustonTXUSA Department of Surgery Weill Cornell Medical College of Cornell UniversityNew YorkNYUSA

The RNA helicase DHX15 is widely expressed in immune cells and traditionally thought to be an RNA splicing factor or a viral RNA ***,the role of DHX15 in NK-cell activities has not been studied thus ***,we generated Dhx15-floxed mice and found that conditional deletion of Dhx15 in NK cells(Ncr1CreDhx15fl/fl mice)resulted in a marked reduction in NK cells in the periphery and that the remaining Dhx15-deleted NK cells failed to acquire a mature *** a result,Dhx15-deleted NK cells exhibited profound defects in their cytolytic *** also found that deletion of Dhx15 in NK cells abrogated their responsiveness to IL-15,which was associated with inhibition of IL-2/IL-15Rβ(CD122)expression and IL-15R *** defects in Dhx15-deleted NK cells were rescued by ectopic expression of a constitutively active form of ***,DHX15 did not affect CD122 mRNA splicing and stability in NK cells but instead facilitated the surface expression of CD122,likely through interaction with its 3′UTR,which was dependent on the ATPase domain of DHX15 rather than its splicing ***,our data identify a key role for DHX15 in regulating NK-cell activities and provide novel mechanistic insights into how DHX15 regulates the IL-15 signaling pathway in NK cells.

关键词： DEAH-box helicase 15(DHX15) Innate immunity Natural killer(NK)cells Homeostasis IL-15 signaling pathway

Infection,Pain,and Itch

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Neuroscience Bulletin 2018年第1期34卷 109-119页

作者： Isaac M.Chiu Department of Microbiology and immunobiology Division of Immunology Harvard Medical School

Pain and itch are unpleasant sensations that often accompany infections caused by viral, bacterial, parasitic, and fungal pathogens. Recent studies show that sensory neurons are able to directly detect pathogens to mediate pain and itch. Nociceptor and pruriceptor neurons respond to pathogen-associated molecular patterns, including Toll-like receptor ligands, N-formyl peptides, and bacterial toxins. Other pathogens are able to silence neuronal activity to produce analgesia during infection. Pain and itch could lead to neuronal modulation of the immune system or behavioral avoidance of future patho- gen exposure. Conversely, pathogens could modulate neuronal signaling to potentiate their pathogenesis and facilitate their spread to other hosts. Defining how pathogens modulate pain and itch has critical implications for sensory neurobiology and our understanding of host- microbe interactions.

关键词： Pain Itch Bacteria Pathogens Infection Inflammation Viruses

Phylogenetic status of Pneumocystis from corticosteroid-treated gerbils

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Science China(Life Sciences) 2010年第10期53卷 1239-1246页

作者： RODNEY D Adam Department of Medicine and immunobiology University of Arizona College of Medicine

Pneumocystis spp. infect the lungs of multiple mammalian species and cause disease in immunosuppressed individuals. The Pneumocystis isolates that have been studied to date fall into two major clades, those from primates and those from rodents. Within each of these clades, different species have been described on the basis of host specificity and differences in sequence and morphology. Here, we demonstrate that dexamethasone immunosuppression consistently results in histologically apparent lung infection in gerbils (28/35 animals). Sequence analysis of the 18S, 5.8S and internal transcribed spacer regions of the rDNA and a portion of the mitochondrial large subunit rDNA demonstrated that this gerbil Pneumocystis is grouped with other rodent Pneumocystis spp., but is distinct from them. Our results suggest that gerbil Pneumocystis differs sufficiently from Pneumocystis species found in other rodents to be considered a separate species.

关键词： 5.8S rRNA gene gerbil internal transcribed spacers (ITS) mitochondrial large subunit (mtLS) rRNA gene 18S rRNA gene Pneumocystis