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https://www.readbyqxmd.com/read/27881606/mitochondria-protection-after-acute-ischemia-prevents-prolonged-upregulation-of-il-1%C3%AE-and-il-18-and-arrests-ckd
#1
Hazel H Szeto, Shaoyi Liu, Yi Soong, Surya V Seshan, Leona Cohen-Gould, Viacheslav Manichev, Leonard C Feldman, Torgny Gustafsson
The innate immune system has been implicated in both AKI and CKD. Damaged mitochondria release danger molecules, such as reactive oxygen species, DNA, and cardiolipin, which can cause NLRP3 inflammasome activation and upregulation of IL-18 and IL-1β It is not known if mitochondrial damage persists long after ischemia to sustain chronic inflammasome activation. We conducted a 9-month study in Sprague-Dawley rats after 45 minutes of bilateral renal ischemia. We detected glomerular and peritubular capillary rarefaction, macrophage infiltration, and fibrosis at 1 month...
November 23, 2016: Journal of the American Society of Nephrology: JASN
https://www.readbyqxmd.com/read/27867381/a-critical-reappraisal-of-neutrophil-extracellular-traps-and-netosis-mimics-based-on-differential-requirements-for-protein-citrullination
#2
Maximilian F Konig, Felipe Andrade
NETosis, an antimicrobial form of neutrophil cell death, is considered a primary source of citrullinated autoantigens in rheumatoid arthritis (RA) and immunogenic DNA in systemic lupus erythematosus (SLE). Activation of the citrullinating enzyme peptidylarginine deiminase type 4 (PAD4) is believed to be essential for neutrophil extracellular trap (NET) formation and NETosis. PAD4 is therefore viewed as a promising therapeutic target to inhibit the formation of NETs in both diseases. In this review, we examine the evidence for PAD4 activation during NETosis and provide experimental data to suggest that protein citrullination is not a universal feature of NETs...
2016: Frontiers in Immunology
https://www.readbyqxmd.com/read/27789101/inflammaging-and-garb-aging
#3
REVIEW
Claudio Franceschi, Paolo Garagnani, Giovanni Vitale, Miriam Capri, Stefano Salvioli
'Inflammaging' refers to the chronic, low-grade inflammation that characterizes aging. Inflammaging is macrophage centered, involves several tissues and organs, including the gut microbiota, and is characterized by a complex balance between pro- and anti-inflammatory responses. Based on literature data, we argue that the major source of inflammatory stimuli is represented by endogenous/self, misplaced, or altered molecules resulting from damaged and/or dead cells and organelles (cell debris), recognized by receptors of the innate immune system...
October 24, 2016: Trends in Endocrinology and Metabolism: TEM
https://www.readbyqxmd.com/read/27636016/mesenchymal-stromal-cells-deficient-in-autophagy-proteins-are-susceptible-to-oxidative-injury-and-mitochondrial-dysfunction
#4
Sailaja Ghanta, Konstantin Tsoyi, Xiaoli Liu, Kiichi Nakahira, Bonna Ith, Anna A Coronata, Laura E Fredenburgh, Joshua A Englert, Claude A Piantadosi, Augustine M K Choi, Mark A Perrella
Oxidative stress resulting from inflammatory responses that occur during acute lung injury and sepsis can initiate changes in mitochondrial function. Autophagy regulates cellular processes in the setting of acute lung injury, sepsis, and oxidative stress by modulating the immune response and facilitating turnover of damaged cellular components. We have shown that mesenchymal stromal cells (MSCs) improve survival in murine models of sepsis by also regulating the immune response. However, the effect of autophagy on MSC and MSC mitochondrial function during oxidative stress is unknown...
September 16, 2016: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/27629285/autophagy-inhibition-and-mitochondrial-remodeling-join-forces-to-amplify-apoptosis-in-activation-induced-cell-death
#5
Corrado Mauro, Campello Silvia
Mitochondrial structural and functional changes and the autophagy pathway crosstalk under several stress conditions. However, their interplay under physiological cell death stimulation has been unclear. In our recent report, we show that during activation-induced cell death (AICD), the T-cell receptor (TCR)-dependent pathway that controls immune tolerance, autophagy is inhibited at an early stage. Further, we found that this inhibition is coupled with mitochondria fragmentation and cristae remodeling to unleash the apoptotic program...
September 14, 2016: Autophagy
https://www.readbyqxmd.com/read/27558401/is-cancer-a-severe-delayed-hypersensitivity-reaction-and-histamine-a-blueprint
#6
Mahin Khatami
Longevity and accumulation of multiple context-dependent signaling pathways of long-standing inflammation (antigen-load or oxidative stress) are the results of decreased/altered regulation of immunity and loss of control switch mechanisms that we defined as Yin and Yang of acute inflammation or immune surveillance. Chronic inflammation is initiated by immune disruptors-induced progressive changes in physiology and function of susceptible host tissues that lead to increased immune suppression and multistep disease processes including carcinogenesis...
December 2016: Clinical and Translational Medicine
https://www.readbyqxmd.com/read/27496003/exposure-to-zidovudine-adversely-affects-mitochondrial-turnover-in-primary-t-cells
#7
Zoë R Wallace, Sharon Sanderson, Anna Katarina Simon, Lucy Dorrell
Zidovudine (ZDV) is a widely used component of antiretroviral therapy (ART) in resource-limited settings, despite its known adverse effects, which include mitochondrial toxicity in muscle, liver and adipose tissue. It has also been associated with impaired immunological recovery. We hypothesised that ZDV might impair mitochondrial health and survival of primary T cells. We performed a cross-sectional analysis of mitochondrial function, mitophagy and susceptibility to apoptosis in healthy donor primary T cells after exposure to ZDV in vitro, together with T cells from patients who were virologically suppressed on ZDV-containing ART regimens for ≥1 year and age-matched subjects receiving non-ZDV ART regimens...
September 2016: Antiviral Research
https://www.readbyqxmd.com/read/27458013/mycotoxin-patulin-suppresses-innate-immune-responses-by-mitochondrial-dysfunction-and-p62-sequestosome-1-dependent-mitophagy
#8
Wan-Ting Tsai, Yin-Chiu Lo, Ming-Sian Wu, Chia-Yang Li, Yi-Ping Kuo, Yi-Hui Lai, Yu Tsai, Kai-Chieh Chen, Tsung-Hsien Chuang, Chun-Hsu Yao, Jinq-Chyi Lee, Li-Chung Hsu, John T-A Hsu, Guann-Yi Yu
Innate immune responses are important for pathogen elimination and adaptive immune response activation. However, excess inflammation may contribute to immunopathology and disease progression (e.g. inflammation-associated hepatocellular carcinoma). Immune modulation resulting from pattern recognition receptor-induced responses is a potential strategy for controlling immunopathology and related diseases. This study demonstrates that the mycotoxin patulin suppresses Toll-like receptor- and RIG-I/MAVS-dependent cytokine production through GSH depletion, mitochondrial dysfunction, the activation of p62-associated mitophagy, and p62-TRAF6 interaction...
September 9, 2016: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/27439607/mitophagy-a-balance-regulator-of-nlrp3-inflammasome-activation
#9
Min-Ji Kim, Joo-Heon Yoon, Ji-Hwan Ryu
The NLRP3 inflammasome is activated by a variety of external or host-derived stimuli and its activation initiates inflammatory response through caspase-1 activation resulting in inflammatory cytokine IL-1β maturation and secretion. The NLRP3 inflammasome activation is a kind of innate immune response most likely mediated by myeloid cells acting as a host defense mechanism. However, if the activation is not properly regulated, excessive inflammation induced by overactivated NLRP3 inflammasome can be detrimental to the host, causing tissue damage and organ dysfunction, eventually causing several diseases...
July 20, 2016: BMB Reports
https://www.readbyqxmd.com/read/27390127/macroautophagy-inhibition-maintains-fragmented-mitochondria-to-foster-t-cell-receptor-dependent-apoptosis
#10
Mauro Corrado, Francesca R Mariotti, Laura Trapani, Lucia Taraborrelli, Francesca Nazio, Valentina Cianfanelli, Maria Eugenia Soriano, Emilie Schrepfer, Francesco Cecconi, Luca Scorrano, Silvia Campello
Mitochondrial dynamics and functionality are linked to the autophagic degradative pathway under several stress conditions. However, the interplay between mitochondria and autophagy upon cell death signalling remains unclear. The T-cell receptor pathway signals the so-called activation-induced cell death (AICD) essential for immune tolerance regulation. Here, we show that this apoptotic pathway requires the inhibition of macroautophagy. Protein kinase-A activation downstream of T-cell receptor signalling inhibits macroautophagy upon AICD induction...
August 15, 2016: EMBO Journal
https://www.readbyqxmd.com/read/27347716/iron-depletion-promotes-mitophagy-to-maintain-mitochondrial-integrity-in-pathogenic-yeast-candida-glabrata
#11
Minoru Nagi, Koichi Tanabe, Hironobu Nakayama, Keigo Ueno, Satoshi Yamagoe, Takashi Umeyama, Hideaki Ohno, Yoshitsugu Miyazaki
Candida glabrata, a haploid budding yeast, is the cause of severe systemic infections in immune-compromised hosts. The amount of free iron supplied to C. glabrata cells during systemic infections is severely limited by iron-chelating proteins such as transferrin. Thus, the iron-deficiency response in C. glabrata cells is thought to play important roles in their survival inside the host's body. In this study, we found that mitophagy was induced under iron-depleted conditions, and that the disruption of a gene homologous to ATG32, which is responsible for mitophagy in Saccharomyces cerevisiae, blocked mitophagy in C...
August 2, 2016: Autophagy
https://www.readbyqxmd.com/read/27345367/parkinson-s-disease-related-proteins-pink1-and-parkin-repress-mitochondrial-antigen-presentation
#12
Diana Matheoud, Ayumu Sugiura, Angélique Bellemare-Pelletier, Annie Laplante, Christiane Rondeau, Magali Chemali, Ali Fazel, John J Bergeron, Louis-Eric Trudeau, Yan Burelle, Etienne Gagnon, Heidi M McBride, Michel Desjardins
Antigen presentation is essential for establishing immune tolerance and for immune responses against infectious disease and cancer. Although antigen presentation can be mediated by autophagy, here we demonstrate a pathway for mitochondrial antigen presentation (MitAP) that relies on the generation and trafficking of mitochondrial-derived vesicles (MDVs) rather than on autophagy/mitophagy. We find that PINK1 and Parkin, two mitochondrial proteins linked to Parkinson's disease (PD), actively inhibit MDV formation and MitAP...
July 14, 2016: Cell
https://www.readbyqxmd.com/read/27133164/fanconi-anemia-proteins-function-in-mitophagy-and-immunity
#13
Rhea Sumpter, Shyam Sirasanagandla, Álvaro F Fernández, Yongjie Wei, Xiaonan Dong, Luis Franco, Zhongju Zou, Christophe Marchal, Ming Yeh Lee, D Wade Clapp, Helmut Hanenberg, Beth Levine
Fanconi anemia (FA) pathway genes are important tumor suppressors whose best-characterized function is repair of damaged nuclear DNA. Here, we describe an essential role for FA genes in two forms of selective autophagy. Genetic deletion of Fancc blocks the autophagic clearance of viruses (virophagy) and increases susceptibility to lethal viral encephalitis. Fanconi anemia complementation group C (FANCC) protein interacts with Parkin, is required in vitro and in vivo for clearance of damaged mitochondria, and decreases mitochondrial reactive oxygen species (ROS) production and inflammasome activation...
May 5, 2016: Cell
https://www.readbyqxmd.com/read/27093228/biology-and-metabolism-of-sepsis-innate-immunity-bioenergetics-and-autophagy
#14
Anthony J Lewis, Timothy R Billiar, Matthew R Rosengart
Sepsis is a complex, heterogeneous physiologic condition that represents a significant public health concern. While many insights into the pathophysiology of sepsis have been elucidated over the past decades of research, important questions remain. This article serves as a review of several important areas in sepsis research. Understanding the innate immune response has been at the forefront as of late, especially in the context of cytokine-directed therapeutic trials. Cellular bioenergetic changes provide insight into the development of organ dysfunction in sepsis...
June 2016: Surgical Infections
https://www.readbyqxmd.com/read/26430570/interfacing-mitochondrial-biogenesis-and-elimination-to-enhance-host-pathogen-defense-and-longevity
#15
Konstantinos Palikaras, Eirini Lionaki, Nektarios Tavernarakis
Mitochondria are highly dynamic and semi-autonomous organelles, essential for many fundamental cellular processes, including energy production, metabolite synthesis and calcium homeostasis, among others. Alterations in mitochondrial activity not only influence individual cell function but also, through non-cell autonomous mechanisms, whole body metabolism, healthspan and lifespan. Energy homeostasis is orchestrated by the complex interplay between mitochondrial biogenesis and mitochondria-selective autophagy (mitophagy)...
July 2015: Worm
https://www.readbyqxmd.com/read/26396268/dichotomous-roles-for-externalized-cardiolipin-in-extracellular-signaling-promotion-of-phagocytosis-and-attenuation-of-innate-immunity
#16
Krishnakumar Balasubramanian, Akihiro Maeda, Janet S Lee, Dariush Mohammadyani, Haider Hussain Dar, Jian Fei Jiang, Claudette M St Croix, Simon Watkins, Vladimir A Tyurin, Yulia Y Tyurina, Katharina Klöditz, Anastassia Polimova, Valentyna I Kapralova, Zeyu Xiong, Prabir Ray, Judith Klein-Seetharaman, Rama K Mallampalli, Hülya Bayir, Bengt Fadeel, Valerian E Kagan
Among the distinct molecular signatures present in the mitochondrion is the tetra-acylated anionic phospholipid cardiolipin, a lipid also present in primordial, single-cell bacterial ancestors of mitochondria and multiple bacterial species today. Cardiolipin is normally localized to the inner mitochondrial membrane; however, when cardiolipin becomes externalized to the surface of dysregulated mitochondria, it promotes inflammasome activation and stimulates the elimination of damaged or nonfunctional mitochondria by mitophagy...
September 22, 2015: Science Signaling
https://www.readbyqxmd.com/read/26287678/memory-nk-cells-take-out-the-mitochondrial-garbage
#17
COMMENT
Julia A Wagner, Todd A Fehniger
The molecular mechanisms important to generate innate natural killer cell "memory" are poorly understood. In this issue of Immunity, O'Sullivan et al. (2015) demonstrate that mitophagy plays a critical role in natural killer cell memory formation following viral infection.
August 18, 2015: Immunity
https://www.readbyqxmd.com/read/26253785/bnip3-and-bnip3l-mediated-mitophagy-promotes-the-generation-of-natural-killer-cell-memory
#18
Timothy E O'Sullivan, Lexus R Johnson, Helen H Kang, Joseph C Sun
Natural killer (NK) cells are innate lymphocytes that possess traits of adaptive immunity, such as clonal expansion, contraction, and generation of long-lived "memory" cells, processes poorly understood at the molecular level. Here, we found that as proliferating NK cells accumulated dysfunctional mitochondria during viral infection, a protective mitophagy pathway was induced during the contraction phase to promote their survival in a reactive oxygen species (ROS)-dependent manner. Inhibition of mechanistic target of rapamycin (mTOR) or activation of AMP-activated protein kinase (AMPK) during the contraction-to-memory phase transition of the antiviral response increased autophagic activity and enhanced memory NK cell numbers through an Atg3-dependent mechanism...
August 18, 2015: Immunity
https://www.readbyqxmd.com/read/26047467/the-evolutionary-history-of-mapl-mitochondria-associated-protein-ligase-and-other-eukaryotic-bam-gide-domain-proteins
#19
Jeremy G Wideman, Blake P Moore
MAPL (mitochondria-associated protein ligase, also called MULAN/GIDE/MUL1) is a multifunctional mitochondrial outer membrane protein found in human cells that contains a unique BAM (beside a membrane) domain and a C-terminal RING-finger domain. MAPL has been implicated in several processes that occur in animal cells such as NF-kB activation, innate immunity and antiviral signaling, suppression of PINK1/parkin defects, mitophagy in skeletal muscle, and caspase-dependent apoptosis. Previous studies demonstrated that the BAM domain is present in diverse organisms in which most of these processes do not occur, including plants, archaea, and bacteria...
2015: PloS One
https://www.readbyqxmd.com/read/25857750/mitophagy-and-the-mitochondrial-unfolded-protein-response-in-neurodegeneration-and-bacterial-infection
#20
REVIEW
Mark W Pellegrino, Cole M Haynes
Mitochondria are highly dynamic and structurally complex organelles that provide multiple essential metabolic functions. Mitochondrial dysfunction is associated with neurodegenerative conditions such as Parkinson's disease, as well as bacterial infection. Here, we explore the roles of mitochondrial autophagy (mitophagy) and the mitochondrial unfolded protein response (UPR(mt)) in the response to mitochondrial dysfunction, focusing in particular on recent evidence on the role of mitochondrial import efficiency in the regulation of these stress pathways and how they may interact to protect the mitochondrial pool while initiating an innate immune response to protect against bacterial pathogens...
2015: BMC Biology
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