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https://www.readbyqxmd.com/read/29787548/a-subset-of-five-human-mitochondrial-formyl-peptides-mimics-bacterial-peptides-and-functionally-deactivates-human-neuetrophils
#1
Elzbieta Kaczmarek, Carl J Hauser, Woon Yong Kwon, Ingred Rica, Li Chen, Nicola Sandler, Leo E Otterbein, Yan Campbell, Charles H Cook, Michael B Yaffe, Michael Marusich, Kiyoshi Itagaki
BACKGROUND: Trauma causes inflammation by releasing mitochondria (MT) that act as DAMPs. Trauma also increases susceptibility to infection. Human MT contain 13 N-formyl peptides (mtFPs). We studied whether mtFPs released into plasma by clinical injury induce neutrophil (PMN) inflammatory responses, whether their potency reflects their similarity to bacterial FPs and how their presence at clinically relevant concentration affects PMN function. METHODS: N-terminal sequences of the 13 mtFPs were synthesized...
May 4, 2018: Journal of Trauma and Acute Care Surgery
https://www.readbyqxmd.com/read/29753511/acute-adrenal-cortex-injury-during-cardiopulmonary-bypass-in-a-canine-model
#2
Bo Mei, Song Yang, Yuan Yue, Jian Hou, Keke Wang, Guangxian Chen, Mengya Liang, Zhongkai Wu
OBJECTIVE: Cardiopulmonary bypass (CPB) might induce systemic inflammatory responses that cause acute injuries to multiple organs. However, no direct evidence exists to determine whether CPB leads to adrenal cortex injury or to describe its underlying mechanism. METHODS: Twelve healthy adult beagles were randomly assigned into control and CPB groups. After cannulation, mild hypothermia CPB was performed in the CPB group but not in the control group. The serum concentrations of various cytokines, cortisol, and aldosterone were assessed...
April 11, 2018: Journal of Thoracic and Cardiovascular Surgery
https://www.readbyqxmd.com/read/29722336/mitochondrial-autophagy-and-nlrp3-inflammasome-in-pulmonary-tissues-from-severe-combined-immunodeficient-mice-after-cardiac-arrest-and-cardiopulmonary-resuscitation
#3
Jing-Jun Lyu, Jawahar L Mehta, Yi Li, Lu Ye, Sheng-Nan Sun, Hong-Shuang Sun, Jia-Chang Li, Dong-Mei Zhang, Jie Wei
Background: The incidence of cancer, diabetes, and autoimmune diseases has been increasing. Furthermore, there are more and more patients with solid organ transplants. The survival rate of these immunocompromised individuals is extremely low when they are severely hit-on. In this study, we established cardiac arrest cardiopulmonary resuscitation (CPR) model in severe combined immunodeficient (SCID) mice, analyzed the expression and activation of mitochondrial autophagy and NLRP3 inflammasome/caspase-1, and explored mitochondrial repair and inflammatory injury in immunodeficiency individual during systemic ischemia-reperfusion injury...
May 20, 2018: Chinese Medical Journal
https://www.readbyqxmd.com/read/29682165/urinary-mitochondrial-dna-identifies-renal-dysfunction-and-mitochondrial-damage-in-sepsis-induced-acute-kidney-injury
#4
Qiongyuan Hu, Jianan Ren, Huajian Ren, Jie Wu, Xiuwen Wu, Song Liu, Gefei Wang, Guosheng Gu, Kun Guo, Jieshou Li
Background: Recent animal studies have shown that mitochondrial dysfunction initiates and accelerates renal injury in sepsis, but its role in sepsis remains unknown. Mitochondrial stress or dying cells can lead to fragmentation of the mitochondrial genome, which is considered a surrogate marker of mitochondrial dysfunction. Therefore, we evaluated the efficiency of urinary mitochondrial DNA (UmtDNA) as a marker of renal dysfunction during sepsis-induced acute kidney injury (AKI). Methods: We isolated DNA from plasma and urine of patients...
2018: Oxidative Medicine and Cellular Longevity
https://www.readbyqxmd.com/read/29658397/inflammation-coagulation-response-and-thrombotic-effects-induced-by-silica-nanoparticles-in-zebrafish-embryos
#5
Junchao Duan, Shuang Liang, Yang Yu, Yang Li, Lijing Wang, Zehao Wu, Yueyue Chen, Mark R Miller, Zhiwei Sun
Nowadays, nanotechnology environmental health and safety (nanoEHS) is gaining attention. We previously found that silica nanoparticles (SiNPs) could induce vascular endothelial damage. However, the subsequent toxicologic response to SiNPs-induced endothelial damage was still largely unknown. In this study, we explored the inflammation-coagulation response and thrombotic effects of SiNPs in endothelial cells and zebrafish embryos. For in vitro study, swollen mitochondria and autophagosome were observed in ultrastructural analysis...
June 2018: Nanotoxicology
https://www.readbyqxmd.com/read/29590639/neutrophil-specific-knockout-demonstrates-a-role-for-mitochondria-in-regulating-neutrophil-motility-in-zebrafish
#6
Wenqing Zhou, Lingyan Cao, Jacob Jeffries, Xiaoguang Zhu, Christopher J Staiger, Qing Deng
Neutrophils are fast-moving cells essential for host immune functions. Although they primarily rely on glycolysis for ATP, isolated primary human neutrophils depend on mitochondrial membrane potential for chemotaxis. However, it is not known whether mitochondria regulate neutrophil motility in vivo , and the underlying molecular mechanisms remain obscure. Here, we visualized mitochondria in an interconnected network that localizes to the front and rear of migrating neutrophils using a novel transgenic zebrafish line...
March 28, 2018: Disease Models & Mechanisms
https://www.readbyqxmd.com/read/29486699/mitochondria-targeted-antioxidant-skq1-10-6%C3%A2-plastoquinonyl-decyltriphenylphosphonium-bromide-inhibits-mast-cell-degranulation-in-vivo-and-in-vitro
#7
M A Chelombitko, O A Averina, T V Vasilyeva, O Yu Pletiushkina, E N Popova, A V Fedorov, B V Chernyak, V S Shishkina, O P Ilinskaya
The therapeutic effect of mitochondria-targeted antioxidant 10-(6´-plastoquinonyl)decyltriphenylphosphonium bromide (SkQ1) in experimental models of acute inflammation and wound repair has been shown earlier. It was suggested that the antiinflammatory activity of SkQ1 is related to its ability to suppress inflammatory activation of the vascular endothelium and neutrophil migration into tissues. Here, we demonstrated that SkQ1 inhibits activation of mast cells (MCs) followed by their degranulation and histamine release in vivo and in vitro...
December 2017: Biochemistry. Biokhimii︠a︡
https://www.readbyqxmd.com/read/29478824/an-unexpected-player-in-gaucher-disease-the-multiple-roles-of-complement-in-disease-development
#8
REVIEW
Manoj K Pandey, Gregory A Grabowski, Jörg Köhl
The complement system is well appreciated for its role as an important effector of innate immunity that is activated by the classical, lectin or alternative pathway. C5a is one important mediator of the system that is generated in response to canonical and non-canonical C5 cleavage by circulating or cell-derived proteases. In addition to its function as a chemoattractant for neutrophils and other myeloid effectors, C5a and its sister molecule C3a have concerted roles in cell homeostasis and surveillance. Through activation of their cognate G protein coupled receptors, C3a and C5a regulate multiple intracellular pathways within the mitochondria and the lysosomal compartments that harbor multiple enzymes critical for protein, carbohydrate and lipid metabolism...
June 2018: Seminars in Immunology
https://www.readbyqxmd.com/read/29467458/maresin-1-attenuates-mitochondrial-dysfunction-through-the-alx-camp-ros-pathway-in-the-cecal-ligation-and-puncture-mouse-model-and-sepsis-patients
#9
Jiaqi Gu, Lingchun Luo, Qian Wang, Songfan Yan, Jing Lin, Dan Li, Bingbing Cao, Hongxia Mei, Binyu Ying, Lu Bin, Fang Gao Smith, Sheng-Wei Jin
Inflammation always accompanies infection during sepsis. Mitochondrial dysfunction and the role of reactive oxygen species (ROS) produced by mitochondria have been proposed in the pathogenesis of sepsis. Maresins have protective and resolving effects in experimental models of infection. In the present study, we investigated the effects of maresin 1 (MaR1) on mitochondrial function in cecal ligation and puncture (CLP)-induced sepsis and sepsis patients to identify mechanisms underlying maresin 1-mediated stimulation of ROS in mitochondria...
February 21, 2018: Laboratory Investigation; a Journal of Technical Methods and Pathology
https://www.readbyqxmd.com/read/29462620/human-ak2-links-intracellular-bioenergetic-redistribution-to-the-fate-of-hematopoietic-progenitors
#10
Koichi Oshima, Norikazu Saiki, Michihiro Tanaka, Hiromi Imamura, Akira Niwa, Ayako Tanimura, Ayako Nagahashi, Akiyoshi Hirayama, Keisuke Okita, Akitsu Hotta, Shuichi Kitayama, Mitsujiro Osawa, Shin Kaneko, Akira Watanabe, Isao Asaka, Wataru Fujibuchi, Kohsuke Imai, Hiromasa Yabe, Yoshiro Kamachi, Junichi Hara, Seiji Kojima, Masaru Tomita, Tomoyoshi Soga, Takafumi Noma, Shigeaki Nonoyama, Tatsutoshi Nakahata, Megumu K Saito
AK2 is an adenylate phosphotransferase that localizes at the intermembrane spaces of the mitochondria, and its mutations cause a severe combined immunodeficiency with neutrophil maturation arrest named reticular dysgenesis (RD). Although the dysfunction of hematopoietic stem cells (HSCs) has been implicated, earlier developmental events that affect the fate of HSCs and/or hematopoietic progenitors have not been reported. Here, we used RD-patient-derived induced pluripotent stem cells (iPSCs) as a model of AK2-deficient human cells...
March 4, 2018: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/29420160/mito-tempo-prevents-nicotine-induced-exacerbation-of-ischemic-brain-damage
#11
Chun Li, Hong Sun, Guodong Xu, Kimberly D McCarter, Jiyu Li, William G Mayhan
Nicotine may contribute to the pathogenesis of cerebrovascular disease via the generation of reactive oxygen species (ROS). Overproduction of ROS leads to brain damage by intensifying post-ischemic inflammation. Our goal was to determine the effect of Mito-Tempo, a mitochondria-targeted antioxidant, on ischemic brain damage and post-ischemic inflammation during chronic exposure to nicotine. Male Sprague-Dawley rats were divided into four groups: control, nicotine, Mito-Tempo-treated control, and Mito-Tempo-treated nicotine...
February 8, 2018: Journal of Applied Physiology
https://www.readbyqxmd.com/read/29295921/lymphocytes-eject-interferogenic-mitochondrial-dna-webs-in-response-to-cpg-and-non-cpg-oligodeoxynucleotides-of-class-c
#12
Björn Ingelsson, Daniel Söderberg, Tobias Strid, Anita Söderberg, Ann-Charlotte Bergh, Vesa Loitto, Kourosh Lotfi, Mårten Segelmark, Giannis Spyrou, Anders Rosén
Circulating mitochondrial DNA (mtDNA) is receiving increasing attention as a danger-associated molecular pattern in conditions such as autoimmunity, cancer, and trauma. We report here that human lymphocytes [B cells, T cells, natural killer (NK) cells], monocytes, and neutrophils derived from healthy blood donors, as well as B cells from chronic lymphocytic leukemia patients, rapidly eject mtDNA as web filament structures upon recognition of CpG and non-CpG oligodeoxynucleotides of class C. The release was quenched by ZnCl2 , independent of cell death (apoptosis, necrosis, necroptosis, autophagy), and continued in the presence of TLR9 signaling inhibitors...
January 16, 2018: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/29132140/mitochondria-targeted-peptide-attenuates-mitochondrial-dysfunction-controls-inflammation-and-protects-against-spinal-cord-injury-induced-lung-injury
#13
Liu-Long Zhu, Mao-Qiang Li, Fan He, Shao-Bo Zhou, Wu Jiang
BACKGROUND/AIMS: Spinal cord injury (SCI) is a common and devastating disease, which results in systemic inflammatory response syndrome and secondary lung injury. Mitochondrial dysfunction and inflammation are closely related to lung injury in diverse disease models. No studies have demonstrated the effects of mitochondrial targeted peptide SS-31 in a mouse model of SCI-induced lung injury. METHODS: Immediately after injury, mice in the treatment groups received a daily, single-dose intraperitoneal injection of SS-31 and for the next 2 days...
2017: Cellular Physiology and Biochemistry
https://www.readbyqxmd.com/read/29081894/the-contribution-of-singlet-oxygen-to-insulin-resistance
#14
REVIEW
Arnold N Onyango
Insulin resistance contributes to the development of diabetes and cardiovascular dysfunctions. Recent studies showed that elevated singlet oxygen-mediated lipid peroxidation precedes and predicts diet-induced insulin resistance (IR), and neutrophils were suggested to be responsible for such singlet oxygen production. This review highlights literature suggesting that insulin-responsive cells such as endothelial cells, hepatocytes, adipocytes, and myocytes also produce singlet oxygen, which contributes to insulin resistance, for example, by generating bioactive aldehydes, inducing endoplasmic reticulum (ER) stress, and modifying mitochondrial DNA...
2017: Oxidative Medicine and Cellular Longevity
https://www.readbyqxmd.com/read/28972154/neutrophil-microparticle-production-and-inflammasome-activation-by-hyperglycemia-due-to-cytoskeletal-instability
#15
Stephen R Thom, Veena M Bhopale, Kevin Yu, Weiliang Huang, Maureen A Kane, David J Margolis
Microparticles are lipid bilayer-enclosed vesicles produced by cells under oxidative stress. MP production is elevated in patients with diabetes, but the underlying cellular mechanisms are poorly understood. We hypothesized that raising glucose above the physiological level of 5.5 mm would stimulate leukocytes to produce MPs and activate the nucleotide-binding domain, leucine-rich repeat pyrin domain-containing 3 (NLRP3) inflammasome. We found that when incubated in buffer with up to 20 mm glucose, human and murine neutrophils, but not monocytes, generate progressively more MPs with high interleukin (IL)-1β content...
November 3, 2017: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/28957874/fracture-healing-and-the-underexposed-role-of-extracellular-vesicle-based-cross-talk
#16
Zhi Qiao, Johannes Greven, Klemens Horst, Roman Pfeifer, Philipp Kobbe, Hans-Christoph Pape, Frank Hildebrand
The process of fracture healing is complex and requires an interaction of multiple organ systems. Cell-cell communication is known to be very important during this process. Extracellular vesicles (EVs) are small membranous vesicles generated from a variety of cells. Proteins, RNAs, small molecules, and mitochondria DNA were found to be transported among cells through EVs. EV-based cross talk represents a substantial cell-cell communication pattern that can both interact with cells through molecular surfaces and transfer molecules to cells...
May 2018: Shock
https://www.readbyqxmd.com/read/28928268/mild-acidosis-delays-neutrophil-apoptosis-via-multiple-signaling-pathways-and-acts-in-concert-with-inflammatory-mediators
#17
Driss El Kebir, Everton de Oliveira Lima Dos Santos, Soukaina Mansouri, Meriem Sekheri, János G Filep
Accumulating evidence indicates development of local extracellular acidosis in inflamed tissues in response to infection and tissue injury. Activation of infiltrating neutrophils contributes to a transient decrease in pH, which, in turn, triggers innate immunity. In this study, we investigated the impact of extracellular acidosis on neutrophil apoptosis, a critical determinant of the outcome of the inflammatory response and analyzed the underlying signaling pathways. Culture of human isolated neutrophils in mildly acidotic conditions (pH 6...
December 2017: Journal of Leukocyte Biology
https://www.readbyqxmd.com/read/28827671/muscle-and-adipose-tissue-morphology-insulin-sensitivity-and-beta-cell-function-in-diabetic-and-nondiabetic-obese-patients-effects-of-bariatric-surgery
#18
Stefania Camastra, Alessandra Vitali, Marco Anselmino, Amalia Gastaldelli, Rosario Bellini, Rossana Berta, Ilenia Severi, Simona Baldi, Brenno Astiarraga, Giorgio Barbatelli, Saverio Cinti, Ele Ferrannini
Obesity is characterized by insulin-resistance (IR), enhanced lipolysis, and ectopic, inflamed fat. We related the histology of subcutaneous (SAT), visceral fat (VAT), and skeletal muscle to the metabolic abnormalities, and tested their mutual changes after bariatric surgery in type 2 diabetic (T2D) and weight-matched non-diabetic (ND) patients. We measured IR (insulin clamp), lipolysis (2 H5 -glycerol infusion), ß-cell glucose-sensitivity (ß-GS, mathematical modeling), and VAT, SAT, and rectus abdominis histology (light and electron microscopy)...
August 21, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28771827/glucocorticoids-the-mode-of-action-in-bullous-pemphigoid
#19
REVIEW
Minna E Kubin, Lars Hellberg, Riitta Palatsi
Bullous pemphigoid (BP) is the most common of pemphigoid diseases caused by autoantibodies against the structures of dermoepidermal junction followed by complement activation, innate immune cell infiltration, neutrophil proteinase secretion and subepidermal blister formation. The first-line treatment of BP is topical and systemic glucocorticoids (GC). Regulation of the immune system and inflammatory cells is the main target of GC actions. GCs act through genomic and non-genomic mechanisms. The human glucocorticoid receptor (GR) mediates most of the biologic effects of GC: cytosolic GR binds GCs and is capable to bind to glucocorticoid response elements in DNA and either transactivate or transrepress genes depending on the tissue and cell type...
December 2017: Experimental Dermatology
https://www.readbyqxmd.com/read/28761623/mitochondria-targeted-antioxidant-skq1-improves-dermal-wound-healing-in-genetically-diabetic-mice
#20
Ilya A Demyanenko, Vlada V Zakharova, Olga P Ilyinskaya, Tamara V Vasilieva, Artem V Fedorov, Vasily N Manskikh, Roman A Zinovkin, Olga Yu Pletjushkina, Boris V Chernyak, Vladimir P Skulachev, Ekaterina N Popova
Oxidative stress is widely recognized as an important factor in the delayed wound healing in diabetes. However, the role of mitochondrial reactive oxygen species in this process is unknown. It was assumed that mitochondrial reactive oxygen species are involved in many wound-healing processes in both diabetic humans and animals. We have applied the mitochondria-targeted antioxidant 10-(6'-plastoquinonyl)decyltriphenylphosphonium (SkQ1) to explore the role of mitochondrial reactive oxygen species in the wound healing of genetically diabetic mice...
2017: Oxidative Medicine and Cellular Longevity
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