scholarly journals Proteinase-Activated Receptor-2 Agonist Activates Anti-Influenza Mechanisms and Modulates IFNγ-Induced Antiviral Pathways in Human Neutrophils

2013 ◽  
Vol 2013 ◽  
pp. 1-10 ◽  
Author(s):  
Micha Feld ◽  
Victoria Shpacovitch ◽  
Christina Ehrhardt ◽  
Michaela Fastrich ◽  
Tobias Goerge ◽  
...  
Keyword(s):  
Influenza A ◽  
Defense Mechanisms ◽  
Inflammatory Diseases ◽  
Human Neutrophils ◽  
Antiviral Resistance ◽  
Antiviral Defense ◽  
Ros Production ◽  
Oxygen Species ◽  
Human Leukocytes ◽  
Antiviral Responses

Proteinase-activated receptor-2 (PAR2) is expressed by human leukocytes and participates in the development of inflammatory diseases. Recent studies demonstrated an ability of PAR2agonist to enhance IFNγ-induced antiviral responses of human leukocytes. However, the precise cellular antiviral defense mechanisms triggered in leukocytes after stimulation with IFNγand/or PAR2agonist remain elusive. Therefore, we aimed to identify neutrophil defense mechanisms involved in antiviral resistance. Here we demonstrated that PAR2agonist enhanced IFNγ-related reduction of influenza A virus (IAV) replication in human neutrophils. PAR2-mediated decrease in IAV replication was associated with reduced NS-1 transcription. Moreover, PAR2-dependent neutrophil activation resulted in enhanced myeloperoxidase degranulation and extracellular myeloperoxidase disrupted IAV. The production of ROS was elevated in response to PAR2activation. Interestingly, IFNγdid not influence both effects: PAR2agonist-triggered myeloperoxidase (MPO) release and reactive oxygen species (ROS) production, which are known to limit IAV infections. In contrast, orthomyxovirus resistance gene A (MxA) protein expression was synergistically elevated through PAR2agonist and IFNγin neutrophils. Altogether, these findings emphasize two PAR2-controlled antiviral mechanisms that are independent of or modulated by IFNγ.

Human neutrophils ROS inhibition and protective effects of Myrtus communis leaves essential oils against intestinal ischemia/reperfusion injury

RSC Advances ◽  
2016 ◽  
Vol 6 (20) ◽  
pp. 16645-16655 ◽  
Author(s):  
Mohamed-Amine Jabri ◽  
Soumaya Hajaji ◽  
Lamjed Marzouki ◽  
Jamel El-Benna ◽  
Mohsen Sakly ◽  
...  
Keyword(s):  
Essential Oils ◽  
Intestinal Ischemia ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Human Neutrophils ◽  
Ros Production ◽  
Oxygen Species ◽  
Protective Effects ◽  
Myrtus Communis ◽  
Intestinal Ischemia Reperfusion

The aim of the present work was to investigate the mechanism implicated in the protective effects ofMyrtus communisleaves essential oils (MCEO) on human neutrophils reactive oxygen species (ROS) production.

scholarly journals IgG-aggregates rapidly up-regulate FcgRI expression at the surface of human neutrophils in a FcgRII-dependent fashion: A crucial role for FcgRI in the generation of reactive oxygen species

2020 ◽  
Author(s):  
Sandrine Huot ◽  
Cynthia Laflamme ◽  
Paul R. Fortin ◽  
Eric Boilard ◽  
Marc Pouliot
Keyword(s):  
Reactive Oxygen Species ◽  
Immune Cells ◽  
Immune Complexes ◽  
Tissue Damage ◽  
Reactive Oxygen ◽  
Surface Expression ◽  
Human Neutrophils ◽  
Ros Production ◽  
Oxygen Species ◽  
Key Players

AbstractAutoimmune complexes are an important feature of several autoimmune diseases such as lupus, as they contribute to tissue damage through the activation of immune cells. Neutrophils, key players in lupus, interact with immune complexes through Fc gamma receptors (FcgR). Incubation of neutrophils with aggregated-IgGs caused degranulation and increased the surface expression of FcgRI within minutes in a concentration-dependent fashion. After 30 min, IgG aggregates (1 mg/ml) up-regulated FcgRI by 4.95 ± 0.45-fold. FcgRI-positive neutrophils reached 67.24% ± 6.88% on HA-IgGs stimulated neutrophils, from 3.12% ± 1.62% in non-stimulated cells, ranking IgG-aggregates among the most potent known agonists. FcgRIIa, and possibly FcgRIIIa, appeared to mediate this up-regulation. Also, FcgRI-dependent signaling proved necessary for reactive oxygen species (ROS) production in response to IgG-aggregates. Finally, combinations of bacterial materials with aggregates dramatically boosted ROS production. This work suggests FcgRI as an essential component in the response of human neutrophils to immune complexes leading to the production of ROS, which may help explain how neutrophils contribute to tissue damage associated with immune complex-associated diseases, such as lupus.

scholarly journals Apocynin: Molecular Aptitudes

2008 ◽  
Vol 2008 ◽  
pp. 1-10 ◽  
Author(s):  
J. Stefanska ◽  
R. Pawliczak
Keyword(s):  
Nadph Oxidase ◽  
Inflammatory Diseases ◽  
Experimental Models ◽  
Ros Production ◽  
Oxygen Species ◽  
Naturally Occurring ◽  
Activated Neutrophils ◽  
Anti Inflammatory ◽  
Insight Into

Apocynin is a naturally occurring methoxy-substituted catechol, experimentally used as an inhibitor of NADPH-oxidase. It can decrease the production of superoxide (O2−) from activated neutrophils and macrophages while the ability of phagocytosis remains unaffected. The anti-inflammatory activity of apocynin has been demonstrated in a variety of cell and animal models of inflammation. Apocynin, after metabolic conversion, inhibits the assembly of NADPH-oxidase that is responsible for reactive oxygen species (ROS) production. It is, therefore, extensively used to reveal the role of this enzyme in cell and experimental models. Although some of the ROS serve as signaling molecules in the cells, excessive production is damaging and has been implicated to play an important role in the progression of many disease processes. This is why in many studies apocynin presents a promising potential treatment for some disorders; however, its utility with inflammatory diseases remains to be determined. Since its mode of action is not well defined, we tried to get a more precise insight into the mechanisms by which apocynin exerts its activity. Considering the anti-inflammatory activities of apocynin, we may conclude that this compound definitely deserves further study.

scholarly journals The prolyl isomerase Pin1 acts as a novel molecular switch for TNF-α–induced priming of the NADPH oxidase in human neutrophils

Blood ◽  
2010 ◽  
Vol 116 (26) ◽  
pp. 5795-5802 ◽  
Author(s):  
Tarek Boussetta ◽  
Marie-Anne Gougerot-Pocidalo ◽  
Gilles Hayem ◽  
Silvia Ciappelloni ◽  
Houssam Raad ◽  
...  
Keyword(s):  
Nadph Oxidase ◽  
Conformational Changes ◽  
Molecular Mechanisms ◽  
Inflammatory Diseases ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Human Neutrophils ◽  
Ros Production ◽  
Prolyl Isomerase ◽  
Tnf Α ◽  
Factor Α

Abstract Neutrophils play a key role in host defense by releasing reactive oxygen species (ROS). However, excessive ROS production by neutrophil nicotinamide adenine dinucleotide phosphate (NADPH) oxidase can damage bystander tissues, thereby contributing to inflammatory diseases. Tumor necrosis factor-α (TNF-α), a major mediator of inflammation, does not activate NADPH oxidase but induces a state of hyperresponsiveness to subsequent stimuli, an action known as priming. The molecular mechanisms by which TNF-α primes the NADPH oxidase are unknown. Here we show that Pin1, a unique cis-trans prolyl isomerase, is a previously unrecognized regulator of TNF-α–induced NADPH oxidase hyperactivation. We first showed that Pin1 is expressed in neutrophil cytosol and that its activity is markedly enhanced by TNF-α. Inhibition of Pin1 activity with juglone or with a specific peptide inhibitor abrogated TNF-α–induced priming of neutrophil ROS production induced by N-formyl-methionyl-leucyl-phenylalanine peptide (fMLF). TNF-α enhanced fMLF-induced Pin1 and p47phox translocation to the membranes and juglone inhibited this process. Pin1 binds to p47phox via phosphorylated Ser345, thereby inducing conformational changes that facilitate p47phox phosphorylation on other sites by protein kinase C. These findings indicate that Pin1 is critical for TNF-α–induced priming of NADPH oxidase and for excessive ROS production. Pin1 inhibition could potentially represent a novel anti-inflammatory strategy.

scholarly journals Carpesium divaricatum Sieb. & Zucc. Revisited: Newly Identified Constituents from Aerial Parts of the Plant and Their Possible Contribution to the Biological Activity of the Plant

Molecules ◽  
2019 ◽  
Vol 24 (8) ◽  
pp. 1614 ◽  
Author(s):  
Natalia Kłeczek ◽  
Barbara Michalak ◽  
Janusz Malarz ◽  
Anna Karolina Kiss ◽  
Anna Stojakowska
Keyword(s):  
Functional Food ◽  
Chemical Constituents ◽  
Human Neutrophils ◽  
Ros Production ◽  
Oxygen Species ◽  
Chlorogenic Acids ◽  
Hydroalcoholic Extract ◽  
Aerial Parts ◽  
History Of ◽  
History Of Use

Carpesium divaricatum Sieb. & Zucc. has a long history of use as both a medicinal and a food plant. However, except for terpenoids, its chemical constituents have remained poorly investigated. The composition of hydroalcoholic extract from aerial parts of C. divaricatum was analyzed by HPLC-DAD-MSn, revealing the presence of numerous caffeic acid derivatives that were formerly unknown constituents of the plant. In all, 17 compounds, including commonly found chlorogenic acids and rarely occurring butyryl and methylbutyryl tricaffeoylhexaric acids, were tentatively identified. Fractionation of lipophilic extract from cultivated shoots led to the isolation of 12-oxo-phytodienoic acid (12-OPDA), which is a newly identified constituent of the plant. The compound, at concentrations of 0.5, 1.0, and 2.5 μM, significantly reduced IL-8, IL-1β, TNFα, and CCL2 excretion by lipopolysaccharide (LPS)-stimulated human neutrophils. Reactive oxygen species (ROS) production induced by f-MLP was also significantly diminished in the neutrophils pretreated by 12-OPDA. The newly identified constituents of the plant seem to be partly responsible for its pharmacological activity and elevate the value of C. divaricatum as a potential functional food.

scholarly journals Assembly of NADPH Oxidase in Human Neutrophils Is Modulated by the Opacity-Associated Protein Expression State of Neisseria gonorrhoeae

2013 ◽  
Vol 82 (3) ◽  
pp. 1036-1044 ◽  
Author(s):  
Asya Smirnov ◽  
Kylene P. Daily ◽  
Alison K. Criss
Keyword(s):  
Reactive Oxygen Species ◽  
Neisseria Gonorrhoeae ◽  
Nadph Oxidase ◽  
Plasma Membranes ◽  
Human Neutrophils ◽  
Ros Production ◽  
Oxygen Species ◽  
Content Type ◽  
The Difference ◽  
Strain Fa1090

ABSTRACTNeisseria gonorrhoeae(the gonococcus, Gc) triggers a potent inflammatory response and recruitment of neutrophils to the site of infection. Gc survives exposure to neutrophils despite these cells' antimicrobial products, such as reactive oxygen species (ROS). ROS production in neutrophils is initiated by NADPH oxidase, which converts oxygen into superoxide. The subunits of NADPH oxidase are spatially separated between granules (gp91phox/p22phox) and the cytoplasm (p47phox, p67phox, and p40phox). Activation of neutrophils promotes the coassembly of NADPH oxidase subunits at phagosome and/or plasma membranes. While Gc-expressing opacity-associated (Opa) proteins can induce neutrophils to produce ROS, Opa-negative (Opa−) Gc does not stimulate neutrophil ROS production. Using constitutively Opa−and OpaD-positive (OpaD+) Gc bacteria in strain FA1090, we now show that the difference in ROS production levels in primary human neutrophils between these backgrounds can be attributed to differential assembly of NADPH oxidase. Neutrophils infected with Opa−Gc showed limited translocation of NADPH oxidase cytoplasmic subunits to cellular membranes, including the bacterial phagosome. In contrast, these subunits rapidly translocated to neutrophil membranes following infection with OpaD+Gc. gp91phoxand p22phoxwere recruited to Gc phagosomes regardless of bacterial Opa expression. These results suggest that Opa−Gc interferes with the recruitment of neutrophil NADPH oxidase cytoplasmic subunits to membranes, in particular, the p47phox“organizing” subunit, to prevent assembly of the holoenzyme, resulting in an absence of the oxidative burst.

scholarly journals Reactive Oxygen Species in Host Plant Are Required for an Early Defense Response against Attack of Stagonospora nodorum Berk. Necrotrophic Effectors SnTox

Plants ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 1586
Author(s):  
Svetlana Veselova ◽  
Tatyana Nuzhnaya ◽  
Guzel Burkhanova ◽  
Sergey Rumyantsev ◽  
Igor Maksimov
Keyword(s):  
Reactive Oxygen Species ◽  
Early Stage ◽  
Reactive Oxygen ◽  
Triticum Aestivum L ◽  
Redox Status ◽  
Stagonospora Nodorum ◽  
Ros Generation ◽  
Ros Production ◽  
Oxygen Species ◽  
Necrotrophic Effectors

Reactive oxygen species (ROS) play a central role in plant immune responses. The most important virulence factors of the Stagonospora nodorum Berk. are multiple fungal necrotrophic effectors (NEs) (SnTox) that affect the redox-status and cause necrosis and/or chlorosis in wheat lines possessing dominant susceptibility genes (Snn). However, the effect of NEs on ROS generation at the early stages of infection has not been studied. We studied the early stage of infection of various wheat genotypes with S nodorum isolates -Sn4VD, SnB, and Sn9MN, carrying a different set of NE genes. Our results indicate that all three NEs of SnToxA, SnTox1, SnTox3 significantly contributed to cause disease, and the virulence of the isolates depended on their differential expression in plants (Triticum aestivum L.). The Tsn1–SnToxA, Snn1–SnTox1and Snn3–SnTox3 interactions played an important role in inhibition ROS production at the initial stage of infection. The Snn3–SnTox3 inhibited ROS production in wheat by affecting NADPH-oxidases, peroxidases, superoxide dismutase and catalase. The Tsn1–SnToxA inhibited ROS production in wheat by affecting peroxidases and catalase. The Snn1–SnTox1 inhibited the production of ROS in wheat by mainly affecting a peroxidase. Collectively, these results show that the inverse gene-for gene interactions between effector of pathogen and product of host sensitivity gene suppress the host’s own PAMP-triggered immunity pathway, resulting in NE-triggered susceptibility (NETS). These results are fundamentally changing our understanding of the development of this economical important wheat disease.

scholarly journals ROS Defense Systems and Terminal Oxidases in Bacteria

Antioxidants ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 839
Author(s):  
Vitaliy B. Borisov ◽  
Sergey A. Siletsky ◽  
Martina R. Nastasi ◽  
Elena Forte
Keyword(s):  
Defense Mechanisms ◽  
Protective Role ◽  
Superoxide Dismutases ◽  
Oxygen Species ◽  
Ros Scavenging ◽  
Terminal Oxidases ◽  
Defense Systems ◽  
Respiratory Chains ◽  
Scavenging Enzymes

Reactive oxygen species (ROS) comprise the superoxide anion (O2·−), hydrogen peroxide (H2O2), hydroxyl radical (·OH), and singlet oxygen (1O2). ROS can damage a variety of macromolecules, including DNA, RNA, proteins, and lipids, and compromise cell viability. To prevent or reduce ROS-induced oxidative stress, bacteria utilize different ROS defense mechanisms, of which ROS scavenging enzymes, such as superoxide dismutases, catalases, and peroxidases, are the best characterized. Recently, evidence has been accumulating that some of the terminal oxidases in bacterial respiratory chains may also play a protective role against ROS. The present review covers this role of terminal oxidases in light of recent findings.

Sign in / Sign up

Export Citation Format

Share Document