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neutrophil mitochondria

Mohamed A A Mahdy, Katsuhiko Warita, Yoshinao Z Hosaka
In this study, we investigated the early changes of skeletal muscle damage in response to injuries induced by cardiotoxin (CTX) and glycerol by using both light microscopy and transmission electron microscopy. Normal, non-dystrophic, adult male mice were used in this study. Tibialis anterior (TA) muscles were injected either with CTX or glycerol. Samples were collected at intervals starting from 1h up to 4days after injury. Injured muscles were subjected to both histological and ultrastructural analyses. CTX-induced injury caused mitochondrial accumulation and swelling followed by lysis, while glycerol-induced injury caused accumulation of vesicles with focal disruption of the basal lamina, indicating that the injuries have different mechanisms of damage to myofibers...
September 28, 2016: Micron: the International Research and Review Journal for Microscopy
Ouahiba Sihali-Beloui, Salima El-Aoufi, Boubekeur Maouche, Sergio Marco
The aim of our transmission electron microscope study was to show, for the first time, the alteration of liver cells involved in the evolution of steatosis to steatohepatitis on a murine model of the diet-induced metabolic syndrome, Psammomys obesus. This pathologic evolution was induced by using the standard laboratory diet during 10 months, and analyzed with metabolic studies and the immunohistochemistry technique. Four months later, hepatocytes charged with lipid vacuoles were involved in autophagy. Furthermore, in the sinusoids, we observed Kupffer cells, neutrophils and macrophages...
September 28, 2016: Comptes Rendus Biologies
Koichiro Sueyoshi, Yuka Sumi, Yoshiaki Inoue, Yoko Kuroda, Kumiko Ishii, Hitoshi Nakayama, Kazuhisa Iwabuchi, Yasutaka Kurishita, Hajime Shigemitsu, Itaru Hamachi, Hiroshi Tanaka
BACKGROUND: The activation of polymorphonuclear neutrophils (PMNs) plays an important role in sepsis. Previously, we showed that ATP release and feedback via ATP receptors are essential for PMN activation; however, the dynamics remain poorly understood. Two new fluorescent chemosensors, PMAP-1 and MitoAP-1, were developed to detect ATP in the plasma membrane and mitochondria of living cells, respectively. In this study, we aimed to evaluate ATP localization using these chemosensors in PMNs of sepsis patients...
December 2016: Annals of Intensive Care
Xuesong Deng, Tongming Deng, Yong Ni, Yongqiang Zhan, Wenlong Huang, Jianfeng Liu, Caixian Liao
It has been observed that polymorphonuclear neutrophils (PMN) increase in number and function during obstructive jaundice (OJ). However, the precise mechanisms underlying PMN apoptosis during OJ remain poorly understood. The aim of the present study was to investigate the modulation of cytochrome c (Cytc) on the mitochondrial signaling pathway in bile duct-ligated (BDL) rats and the effect on PMN apoptosis following the intravenous administration of Cytc. Rats were randomly divided into four groups: A control group, a sham group, a BDL group and a BDL + Cytc group (rats with common bile duct ligation as well as Cytc intravenous injection)...
July 2016: Experimental and Therapeutic Medicine
Claes Dahlgren, Michael Gabl, André Holdfeldt, Malene Winther, Huamei Forsman
Proper recruitment and activation of neutrophils to/at sites of infection/inflammation relies largely on the surface expression of chemoattractant receptors of which a formyl peptide receptor (FPR1) was the first to be cloned and characterized in more detail. This receptor displays high affinity for bacterial- or mitochondrial-derived peptides that contain a formylated methionine in the N-terminus. The neutrophil chemoattractant receptors belong to the group of 7-transmembrane domain receptors that signal through activation of heterotrimeric G proteins...
August 15, 2016: Biochemical Pharmacology
Simone Caielli, Shruti Athale, Bojana Domic, Elise Murat, Manjari Chandra, Romain Banchereau, Jeanine Baisch, Kate Phelps, Sandra Clayton, Mei Gong, Tracey Wright, Marilynn Punaro, Karolina Palucka, Cristiana Guiducci, Jacques Banchereau, Virginia Pascual
Autoantibodies against nucleic acids and excessive type I interferon (IFN) are hallmarks of human systemic lupus erythematosus (SLE). We previously reported that SLE neutrophils exposed to TLR7 agonist autoantibodies release interferogenic DNA, which we now demonstrate to be of mitochondrial origin. We further show that healthy human neutrophils do not complete mitophagy upon induction of mitochondrial damage. Rather, they extrude mitochondrial components, including DNA (mtDNA), devoid of oxidized (Ox) residues...
May 2, 2016: Journal of Experimental Medicine
P Mikolka, J Kopincova, L Tomcikova Mikusiakova, P Kosutova, M Antosova, A Calkovska, D Mokra
Meconium aspiration syndrome (MAS) is a serious condition, which can be treated with exogenous surfactant and mechanical ventilation. However, meconium-induced inflammation, lung edema and oxidative damage may inactivate delivered surfactant and thereby reduce effectiveness of the therapy. As we presumed that addition of anti-inflammatory agent into the surfactant may alleviate inflammation and enhance efficiency of the therapy, this study was performed to evaluate effects of surfactant therapy enriched with budesonide versus surfactant-only therapy on markers of oxidative stress in experimental model of MAS...
February 2016: Journal of Physiology and Pharmacology: An Official Journal of the Polish Physiological Society
Pan Zhang, David C Samuels, Jing Wang, Shilin Zhao, Yu Shyr, Yan Guo
It has been shown that heteroplasmic mitochondrial DNA variants can be tissue specific. However, whether mitochondrial DNA variants are specific by blood cell types has not been investigated. Motivated by this question and using mitochondria sequences extracted from RNAseq data from six distinct blood cell types (neutrophil, monocyte, myeloid dendritic, natural killer, T and B), we thoroughly compared SNPs and heteroplasmies among these cell types. Each cell type from each subject was sequenced at four time points used as biological replicates...
May 2016: Mitochondrion
Song Liu, Min Feng, Wenxian Guan
Recent studies have revealed the diverse pathophysiological functions of mitochondria beyond traditional energetic metabolism in cells. Mitochondria-released damage-associated molecular patterns, particularly mitochondrial deoxyribonucleic acid (mtDNA), play a central role in host immune defenses against foreign pathogens. Newly discovered cGAS-STING signaling is responsible for microbial DNA recognition, and potentially participates in mitochondrial DNA sensing. Inappropriate inflammatory signaling mediated by mtDNA is implicated in various human diseases, especially infectious/inflammatory disease and cancer...
August 15, 2016: International Journal of Cancer. Journal International du Cancer
Kazuta Yasui, Nobuki Matsuyama, Ayumu Kuroishi, Yoshihiko Tani, Rika A Furuta, Fumiya Hirayama
BACKGROUND: Platelet concentrates (PCs) are the most common blood components eliciting nonhemolytic transfusion reactions (NHTRs), such as allergic transfusion reactions and febrile reactions. However, the precise mechanisms of NHTRs in PC transfusion remain largely unknown. Previous studies reported that mitochondria-derived damage-associated molecular patterns (DAMPs) could be important mediators of innate cell inflammation. Platelets (PLTs) represent a major reservoir of mitochondria in the blood circulation...
May 2016: Transfusion
Jenna M McCracken, Lauren C Kinkead, Ramona L McCaffrey, Lee-Ann H Allen
Tularemia is a disease characterized by profound neutrophil accumulation and tissue destruction. The causative organism, Francisella tularensis, is a facultative intracellular bacterium that replicates in neutrophil cytosol, inhibits caspase activation and profoundly prolongs cell lifespan. Here, we identify unique features of this infection and provide fundamental insight into the mechanisms of apoptosis inhibition. Mitochondria are critical regulators of neutrophil apoptosis. We demonstrate that F. tularensis significantly inhibits Bax translocation and Bid processing during 24-48 h of infection, and in this manner sustains mitochondrial integrity...
2016: Journal of Innate Immunity
Takahiro Moriyama, Yuichi Kanmura, Sten G E Lindahl
BACKGROUND: Ischemia-reperfusion (I/R) injury is one of the most important pathologic processes causing acute kidney injury. Human atrial natriuretic peptide (hANP) has various effects, including renal protection. The purpose of the present work was to study the effects of intrarenal angiotensin II (Ang II) and investigate the potential of hANP to prevent kidney injury. MATERIALS AND METHODS: Male Sprague-Dawley rats were divided into three groups as follows: (1) sham; (2) I/R (30 min of bilateral renal ischemia followed by 6 h reperfusion); and (3) I/R + hANP (I/R injury + continuous intravenous infusion of hANP at 0...
March 2016: Journal of Surgical Research
Jonathan Arauz, Erika Ramos-Tovar, Pablo Muriel
 Oxidative stress is importantly involved in the pathophysiology of various liver diseases. The redox state participates on the course of the inflammatory, metabolic and proliferative liver diseases. The main sources of the reactive oxygen species (ROS) are represented by the mitochondria and cytochrome P450 enzymes in the hepatocyte, Kupffer cells and neutrophils. Cells are provided with efficient molecular strategies to strictly control the intracellular ROS level and to maintain the balance between oxidant and antioxidant molecules...
March 2016: Annals of Hepatology
Christian Lood, Luz P Blanco, Monica M Purmalek, Carmelo Carmona-Rivera, Suk S De Ravin, Carolyne K Smith, Harry L Malech, Jeffrey A Ledbetter, Keith B Elkon, Mariana J Kaplan
Neutrophil extracellular traps (NETs) are implicated in autoimmunity, but how they are generated and their roles in sterile inflammation remain unclear. Ribonucleoprotein immune complexes (RNP ICs), inducers of NETosis, require mitochondrial reactive oxygen species (ROS) for maximal NET stimulation. After RNP IC stimulation of neutrophils, mitochondria become hypopolarized and translocate to the cell surface. Extracellular release of oxidized mitochondrial DNA is proinflammatory in vitro, and when this DNA is injected into mice, it stimulates type I interferon (IFN) signaling through a pathway dependent on the DNA sensor STING...
February 2016: Nature Medicine
Alexandra Gennaris, Benjamin Ezraty, Camille Henry, Rym Agrebi, Alexandra Vergnes, Emmanuel Oheix, Julia Bos, Pauline Leverrier, Leon Espinosa, Joanna Szewczyk, Didier Vertommen, Olga Iranzo, Jean-François Collet, Frédéric Barras
The reactive species of oxygen and chlorine damage cellular components, potentially leading to cell death. In proteins, the sulfur-containing amino acid methionine is converted to methionine sulfoxide, which can cause a loss of biological activity. To rescue proteins with methionine sulfoxide residues, living cells express methionine sulfoxide reductases (Msrs) in most subcellular compartments, including the cytosol, mitochondria and chloroplasts. Here we report the identification of an enzymatic system, MsrPQ, repairing proteins containing methionine sulfoxide in the bacterial cell envelope, a compartment particularly exposed to the reactive species of oxygen and chlorine generated by the host defence mechanisms...
December 17, 2015: Nature
Bartosz Szczesny, Attila Brunyánszki, Akbar Ahmad, Gabor Oláh, Craig Porter, Tracy Toliver-Kinsky, Labros Sidossis, David N Herndon, Csaba Szabo
Severe thermal injury induces a pathophysiological response that affects most of the organs within the body; liver, heart, lung, skeletal muscle among others, with inflammation and hyper-metabolism as a hallmark of the post-burn damage. Oxidative stress has been implicated as a key component in development of inflammatory and metabolic responses induced by burn. The goal of the current study was to evaluate several critical mitochondrial functions in a mouse model of severe burn injury. Mitochondrial bioenergetics, measured by Extracellular Flux Analyzer, showed a time dependent, post-burn decrease in basal respiration and ATP-turnover but enhanced maximal respiratory capacity in mitochondria isolated from the liver and lung of animals subjected to burn injury...
2015: PloS One
Takayuki Marutani, Tatsuya Hattori, Koki Tsutsumi, Yusuke Koike, Akihiko Harada, Kosuke Noguchi, Yoshiaki Kiso, Hidehito Mukai
Recently, much attention has been paid to "nonclassical" bioactive peptides, which are fragmented peptides simultaneously produced during maturation and degradation of various functional proteins. We identified many fragmented peptides derived from various mitochondrial proteins including mitocryptide-1 and mitocryptide-2 that efficiently activate neutrophils. These endogenous, functionally active, fragmented peptides are referred to as "cryptides." Among them, mitocryptide-2 is an N-formylated cryptide cleaved from mitochondrial cytochrome b that is encoded in mitochondrial DNA (mtDNA)...
November 4, 2016: Biopolymers
Jon Hazeldine, Janet M Lord, Antonio Belli
Nosocomial infections are a common occurrence in patients following traumatic brain injury (TBI) and are associated with an increased risk of mortality, longer length of hospital stay, and poor neurological outcome. Systemic immune suppression arising as a direct result of injury to the central nervous system (CNS) is considered to be primarily responsible for this increased incidence of infection, a view strengthened by recent studies that have reported novel changes in the composition and function of the innate and adaptive arms of the immune system post-TBI...
2015: Frontiers in Neurology
Edwin K Jackson, Elizabeth V Menshikova, Zaichuan Mi, Jonathan D Verrier, Rashmi Bansal, Keri Janesko-Feldman, Travis C Jackson, Patrick M Kochanek
A positional isomer of 3',5'-cAMP, 2',3'-cAMP, is produced by kidneys in response to energy depletion, and renal 2',3'-cyclic nucleotide 3'-phosphodiesterase (CNPase) metabolizes 2',3'-cAMP to 2'-AMP; 2',3'-cAMP is a potent opener of mitochondrial permeability transition pores (mPTPs), which can stimulate autophagy. Because autophagy protects against AKI, it is conceivable that inhibition of CNPase protects against ischemia-reperfusion (IR) -induced AKI. Therefore, we investigated renal outcomes, mitochondrial function, number, area, and autophagy in CNPase-knockout (CNPase(-/-)) versus wild-type (WT) mice using a unique two-kidney, hanging-weight model of renal bilateral IR (20 minutes of ischemia followed by 48 hours of reperfusion)...
July 2016: Journal of the American Society of Nephrology: JASN
Akbar Ahmad, Gabor Olah, Bartosz Szczesny, Mark E Wood, Matthew Whiteman, Csaba Szabo
This study evaluated the effects of AP39 [(10-oxo-10-(4-(3-thioxo-3H-1,2-dithiol-5yl) phenoxy)decyl) triphenyl phosphonium bromide], a mitochondrially targeted donor of hydrogen sulfide (H2S) in an in vitro model of hypoxia/oxidative stress injury in NRK-49F rat kidney epithelial cells (NRK cells) and in a rat model of renal ischemia-reperfusion injury. Renal oxidative stress was induced by the addition of glucose oxidase, which generates hydrogen peroxide in the culture medium at a constant rate. Glucose oxidase (GOx)-induced oxidative stress led to mitochondrial dysfunction, decreased intracellular ATP content, and, at higher concentrations, increased intracellular oxidant formation (estimated by the fluorescent probe 2, 7-dichlorofluorescein, DCF) and promoted necrosis (estimated by the measurement of lactate dehydrogenase release into the medium) of the NRK cells in vitro...
January 2016: Shock
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