scholarly journals Mitochondrial Reactive Oxygen Species Regulate Immune Responses of Macrophages to Aspergillus fumigatus

2021 ◽  
Vol 12 ◽  
Author(s):  
Remi Hatinguais ◽  
Arnab Pradhan ◽  
Gordon D. Brown ◽  
Alistair J. P. Brown ◽  
Adilia Warris ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Aspergillus Fumigatus ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Mitochondrial Ros ◽  
Tnf Α ◽  
Reverse Electron Transport ◽  
Phagosomal Membrane ◽  
Antimicrobial Immunity

Reactive Oxygen Species (ROS) are highly reactive molecules that can induce oxidative stress. For instance, the oxidative burst of immune cells is well known for its ability to inhibit the growth of invading pathogens. However, ROS also mediate redox signalling, which is important for the regulation of antimicrobial immunity. Here, we report a crucial role of mitochondrial ROS (mitoROS) in antifungal responses of macrophages. We show that mitoROS production rises in murine macrophages exposed to swollen conidia of the fungal pathogen Aspergillus fumigatus compared to untreated macrophages, or those treated with resting conidia. Furthermore, the exposure of macrophages to swollen conidia increases the activity of complex II of the respiratory chain and raises mitochondrial membrane potential. These alterations in mitochondria of infected macrophages suggest that mitoROS are produced via reverse electron transport (RET). Significantly, preventing mitoROS generation via RET by treatment with rotenone, or a suppressor of site IQ electron leak, S1QEL1.1, lowers the production of pro-inflammatory cytokines TNF-α and IL-1β in macrophages exposed to swollen conidia of A. fumigatus. Rotenone and S1QEL1.1 also reduces the fungicidal activity of macrophages against swollen conidia. Moreover, we have established that elevated recruitment of NADPH oxidase 2 (NOX2, also called gp91phox) to the phagosomal membrane occurs prior to the increase in mitoROS generation. Using macrophages from gp91phox-/- mice, we have further demonstrated that NOX2 is required to regulate cytokine secretion by RET-associated mitoROS in response to infection with swollen conidia. Taken together, these observations demonstrate the importance of RET-mediated mitoROS production in macrophages infected with A. fumigatus.

Role of Reactive Oxygen Species and Bcl-2 Family Proteins in TNF-α-Induced Apoptosis of Lymphocytes

2010 ◽  
Vol 149 (2) ◽  
pp. 180-183 ◽  
Author(s):  
N. V. Ryazanceva ◽  
V. V. Novickiy ◽  
O. B. Zhukova ◽  
A. K. Biktasova ◽  
O. E. Chechina ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Tnf Α ◽  
Induced Apoptosis

scholarly journals Comparing Early Eukaryotic Integration of Mitochondria and Chloroplasts in the Light of Internal ROS Challenges: Timing is of the Essence

mBio ◽  
2020 ◽  
Vol 11 (3) ◽  
Author(s):  
Dave Speijer ◽  
Michael Hammond ◽  
Julius Lukeš
Keyword(s):  
Reactive Oxygen Species ◽  
Driving Forces ◽  
Reactive Oxygen ◽  
High Energy ◽  
Oxygen Species ◽  
Mitochondrial Ros ◽  
Transport Chain ◽  
Evolutionary Trajectories ◽  
Ros Formation

ABSTRACT When trying to reconstruct the evolutionary trajectories during early eukaryogenesis, one is struck by clear differences in the developments of two organelles of endosymbiotic origin: the mitochondrion and the chloroplast. From a symbiogenic perspective, eukaryotic development can be interpreted as a process in which many of the defining eukaryotic characteristics arose as a result of mutual adaptions of both prokaryotes (an archaeon and a bacterium) involved. This implies that many steps during the bacterium-to-mitochondrion transition trajectory occurred in an intense period of dramatic and rapid changes. In contrast, the subsequent cyanobacterium-to-chloroplast development in a specific eukaryotic subgroup, leading to the photosynthetic lineages, occurred in a full-fledged eukaryote. The commonalities and differences in the two trajectories shed an interesting light on early, and ongoing, eukaryotic evolutionary driving forces, especially endogenous reactive oxygen species (ROS) formation. Differences between organellar ribosomes, changes to the electron transport chain (ETC) components, and mitochondrial codon reassignments in nonplant mitochondria can be understood when mitochondrial ROS formation, e.g., during high energy consumption in heterotrophs, is taken into account. IMPORTANCE The early eukaryotic evolution was deeply influenced by the acquisition of two endosymbiotic organelles - the mitochondrion and the chloroplast. Here we discuss the possibly important role of reactive oxygen species in these processes.

scholarly journals The Role of Reactive Oxygen Species in the Pathogenesis of Adipocyte Dysfunction in Metabolic Syndrome. Prospects of Pharmacological Correction

2017 ◽  
Vol 72 (1) ◽  
pp. 11-16 ◽  
Author(s):  
E. S. Prokudina ◽  
L. N. Maslov ◽  
V. V. Ivanov ◽  
I. D. Bespalova ◽  
D. S. Pismennyi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Reactive Oxygen Species ◽  
Metabolic Syndrome ◽  
Positive Impact ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Tnf Α ◽  
The One

It is established that oxidative stress induces insulin resistance of adipocytes, increases secretion leptin, IL-6, TNF-α by adipocytes. Adiponectin secretion by adipocytes is reduced after the action of reactive oxygen species. Metabolic syndrome contributes to oxidative stress in adipose tissue, on the one hand due to the activation of production of reactive oxygen species by adipocyte NADPH-oxidase, and on the other hand by reducing the antioxidant defense adipocytes. It is found that obesity itself can induce oxidative stress. Chronic stress, glucocorticoids, mineralocorticoids, angiotensin-II, TNF-α play an important role in the pathogenesis of oxidative stress of adipocytes. Metformin remains the cure for the treatment of insulin resistance. The positive results in the treatment of metabolic syndrome by losartan were obtained. Antioxidants and flavonoids exhibit a positive impact on the course of the experimental metabolic syndrome.

Role of reactive oxygen species and antioxidants in periodontal disease

2021 ◽  
pp. 1-16
Author(s):  
Harish M. Saluja ◽  
Shivani Sachdeva ◽  
Amit Mani
Keyword(s):  
Reactive Oxygen Species ◽  
Periodontal Disease ◽  
Bacterial Species ◽  
Reactive Oxygen ◽  
Epidemiological Studies ◽  
Oxygen Species ◽  
Tissue Destruction ◽  
Tnf Α ◽  
Harmful Effects

Recent epidemiological studies reveal that more than two-third of the world’s population suffers from one of the chronic forms of periodontal disease. The primary etiological agent of this inflammatory disease is a polymicrobial complex, predominantly Gram negative anaerobic or facultative bacteria within the sub-gingival biofilm. These bacterial species initiate the production of various cytokines such as interleukin-8 and TNF-α, further causing an increase in number and activity of polymorphonucleocytes (PMN) along with these cytokines, PMNs also produce reactive oxygen species (ROS) superoxide via the respiratory burst mechanism as the part of the defence response to infection. ROS just like the interleukins have deleterious effects on tissue cells when produced in excess. To counter the harmful effects of ROS, human body has its own defence mechanisms to eliminate them as soon as they are formed. The aim of this review is to focus on the role of different free radicals, ROS, and antioxidants in the pathophysiology of periodontal tissue destruction.

Regulation of intrinsic prion protein by growth factors and tnf-α: the role of intracellular reactive oxygen species

2003 ◽  
Vol 35 (6) ◽  
pp. 586-594 ◽  
Author(s):  
Heinrich Sauer ◽  
Katrin Wefer ◽  
Vito Vetrugno ◽  
Maurizio Pocchiari ◽  
Cornelia Gissel ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Growth Factors ◽  
Prion Protein ◽  
Reactive Oxygen ◽  
Intracellular Reactive Oxygen Species ◽  
Oxygen Species ◽  
Tnf Α

scholarly journals Reactive oxygen species promote tubular injury in diabetic nephropathy: The role of the mitochondrial ros-txnip-nlrp3 biological axis

Redox Biology ◽  
2018 ◽  
Vol 16 ◽  
pp. 32-46 ◽  
Author(s):  
Yachun Han ◽  
Xiaoxuan Xu ◽  
Chengyuan Tang ◽  
Peng Gao ◽  
Xianghui Chen ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Diabetic Nephropathy ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Tubular Injury ◽  
Mitochondrial Ros

Mitochondrial reactive oxygen species-mediated signaling in endothelial cells

2007 ◽  
Vol 292 (5) ◽  
pp. H2023-H2031 ◽  
Author(s):  
David X. Zhang ◽  
David D. Gutterman
Keyword(s):  
Reactive Oxygen Species ◽  
Endothelial Cells ◽  
Cell Signaling ◽  
Vascular Endothelial Cells ◽  
Reactive Oxygen ◽  
Vascular Endothelial ◽  
Ros Production ◽  
Oxygen Species ◽  
Mitochondrial Ros

Once thought of as toxic by-products of cellular metabolism, reactive oxygen species (ROS) have been implicated in a large variety of cell-signaling processes. Several enzymatic systems contribute to ROS production in vascular endothelial cells, including NA(D)PH oxidase, xanthine oxidase, uncoupled endothelial nitric oxide synthase, and the mitochondrial electron transport chain. The respiratory chain is the major source of ROS in most mammalian cells, but the role of mitochondria-derived ROS in vascular cell signaling has received little attention. A new paradigm has evolved in recent years postulating that, in addition to producing ATP, mitochondria also play a key role in cell signaling and regulate a variety of cellular functions. This review focuses on the emerging role of mitochondrial ROS as signaling molecules in vascular endothelial cells. Specifically, we discuss some recent findings that indicate that mitochondrial ROS regulate vascular endothelial function, focusing on major sites of ROS production in endothelial mitochondria, factors modulating mitochondrial ROS production, the physiological and clinical implications of endothelial mitochondrial ROS, and methodological considerations in the study of mitochondrial contribution to vascular ROS generation.

scholarly journals Reactive Oxygen Species in Macrophages: Sources and Targets

2021 ◽  
Vol 12 ◽  
Author(s):  
Marcella Canton ◽  
Ricardo Sánchez-Rodríguez ◽  
Iolanda Spera ◽  
Francisca C. Venegas ◽  
Maria Favia ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Signaling Networks ◽  
Oxygen Species ◽  
Cellular Processes ◽  
Pathological Conditions ◽  
Mitochondrial Ros ◽  
Ros Formation ◽  
Excessive Accumulation

Reactive oxygen species (ROS) are fundamental for macrophages to eliminate invasive microorganisms. However, as observed in nonphagocytic cells, ROS play essential roles in processes that are different from pathogen killing, as signal transduction, differentiation, and gene expression. The different outcomes of these events are likely to depend on the specific subcellular site of ROS formation, as well as the duration and extent of ROS production. While excessive accumulation of ROS has long been appreciated for its detrimental effects, there is now a deeper understanding of their roles as signaling molecules. This could explain the failure of the “all or none” pharmacologic approach with global antioxidants to treat several diseases. NADPH oxidase is the first source of ROS that has been identified in macrophages. However, growing evidence highlights mitochondria as a crucial site of ROS formation in these cells, mainly due to electron leakage of the respiratory chain or to enzymes, such as monoamine oxidases. Their role in redox signaling, together with their exact site of formation is only partially elucidated. Hence, it is essential to identify the specific intracellular sources of ROS and how they influence cellular processes in both physiological and pathological conditions to develop therapies targeting oxidative signaling networks. In this review, we will focus on the different sites of ROS formation in macrophages and how they impact on metabolic processes and inflammatory signaling, highlighting the role of mitochondrial as compared to non-mitochondrial ROS sources.

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