The impact of endocrine-disrupting chemicals on oxidative stress and innate immune response in zebrafish embryos

2013 ◽  
Vol 32 (8) ◽  
pp. 1793-1799 ◽  
Author(s):  
Hai Xu ◽  
Ming Yang ◽  
Wenhui Qiu ◽  
Chenyuan Pan ◽  
Minghong Wu
Keyword(s):  
Oxidative Stress ◽  
Immune Response ◽  
Innate Immune Response ◽  
Endocrine Disrupting Chemicals ◽  
Innate Immune ◽  
Zebrafish Embryos ◽  
Endocrine Disrupting ◽  
The Impact

Effects of triclocarban on oxidative stress and innate immune response in zebrafish embryos

Chemosphere ◽  
2018 ◽  
Vol 210 ◽  
pp. 93-101 ◽  
Author(s):  
Jiajing Wei ◽  
Ting Zhou ◽  
Zhiyong Hu ◽  
Ying Li ◽  
Hongfang Yuan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Immune Response ◽  
Innate Immune Response ◽  
Innate Immune ◽  
Zebrafish Embryos

scholarly journals Innate Immune Response of Human Embryonic Stem Cell-Derived Fibroblasts and Mesenchymal Stem Cells to Periodontopathogens

2016 ◽  
Vol 2016 ◽  
pp. 1-15 ◽  
Author(s):  
Gopu Sriram ◽  
Vaishali Prakash Natu ◽  
Intekhab Islam ◽  
Xin Fu ◽  
Chaminda Jayampath Seneviratne ◽  
...  
Keyword(s):  
Stem Cells ◽  
Immune Response ◽  
Mesenchymal Stem Cells ◽  
Innate Immune Response ◽  
Embryonic Stem ◽  
Innate Immune ◽  
Microbial Pathogens ◽  
Multipotent Stem Cells ◽  
Cytokine Expression Profile ◽  
The Impact

Periodontitis involves complex interplay of bacteria and host immune response resulting in destruction of supporting tissues of the tooth. Toll-like receptors (TLRs) play a role in recognizing microbial pathogens and eliciting an innate immune response. Recently, the potential application of multipotent stem cells and pluripotent stem cells including human embryonic stem cells (hESCs) in periodontal regenerative therapy has been proposed. However, little is known about the impact of periodontopathogens on hESC-derived progenies. This study investigates the effects of heat-killed periodontopathogens, namely,Porphyromonas gingivalisandAggregatibacter actinomycetemcomitans, on TLR and cytokine expression profile of hESC-derived progenies, namely, fibroblasts (hESC-Fib) and mesenchymal stem cells (hESC-MSCs). Additionally, the serotype-dependent effect ofA. actinomycetemcomitanson hESC-derived progenies was explored. Both hESC-Fib and hESC-MSCs constitutively expressedTLR-2andTLR-4. hESC-Fib upon exposure to periodontopathogens displayed upregulation of TLRs and release of cytokines (IL-1β, IL-6, and IL-8). In contrast, hESC-MSCs were largely nonresponsive to bacterial challenge, especially in terms of cytokine production. Further, exposure of hESC-Fib toA. actinomycetemcomitansserotype c was associated with higher IL-8 production than serotype b. In contrast, the hESC-MSCs displayed no serotype-dependent response. Differential response of the two hESC progenies implies a phenotype-dependent response to periodontopathogens and supports the concept of immunomodulatory properties of MSCs.

scholarly journals Rubella Virus Strain-Associated Differences in the Induction of Oxidative Stress Are Independent of Their Interferon Activation

Viruses ◽  
2018 ◽  
Vol 10 (10) ◽  
pp. 540 ◽  
Author(s):  
Sarah Zobel ◽  
Mechthild Lorenz ◽  
Giada Frascaroli ◽  
Janik Böhnke ◽  
Nicole Bilz ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Immune Response ◽  
Innate Immune Response ◽  
Rubella Virus ◽  
Gene Activation ◽  
Innate Immune ◽  
Clinical Isolates ◽  
Stress Induction ◽  
Mitochondrial Superoxide ◽  
Mitochondrial Ros

Rubella virus (RV) infection impacts cellular metabolic activity in a complex manner with strain-specific nutritional requirements. Here we addressed whether this differential metabolic influence was associated with differences in oxidative stress induction and subsequently with innate immune response activation. The low passaged clinical isolates of RV examined in this study induced oxidative stress as validated through generation of the reactive oxygen species (ROS) cytoplasmic hydrogen peroxide and mitochondrial superoxide. The addition of the cytoplasmic and mitochondrial ROS scavengers N-acetyl-l-cysteine and MitoTEMPO, respectively, reduced RV-associated cytopathogenicity and caspase activation. While the degree of oxidative stress induction varied among RV clinical isolates, the level of innate immune response and interferon-stimulated gene activation was comparable. The type III IFNs were highly upregulated in all cell culture systems tested. However, only pre-stimulation with IFN β slightly reduced RV replication indicating that RV appears to have evolved the ability to counteract innate immune response mechanisms. Through the data presented, we showed that the ability of RV to induce oxidative stress was independent of its capacity to stimulate and counteract the intrinsic innate immune response.

scholarly journals The transcription factor NRF2 enhances melanoma malignancy by blocking differentiation and inducing COX2 expression

Oncogene ◽  
2020 ◽  
Vol 39 (44) ◽  
pp. 6841-6855 ◽  
Author(s):  
Christina Jessen ◽  
Julia K. C. Kreß ◽  
Apoorva Baluapuri ◽  
Anita Hufnagel ◽  
Werner Schmitz ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Immune Response ◽  
Transcription Factor ◽  
Prostaglandin E2 ◽  
Innate Immune Response ◽  
Stress Responses ◽  
Melanoma Cells ◽  
Innate Immune ◽  
Dependent Manner

AbstractThe transcription factor NRF2 is the major mediator of oxidative stress responses and is closely connected to therapy resistance in tumors harboring activating mutations in the NRF2 pathway. In melanoma, such mutations are rare, and it is unclear to what extent melanomas rely on NRF2. Here we show that NRF2 suppresses the activity of the melanocyte lineage marker MITF in melanoma, thereby reducing the expression of pigmentation markers. Intriguingly, we furthermore identified NRF2 as key regulator of immune-modulating genes, linking oxidative stress with the induction of cyclooxygenase 2 (COX2) in an ATF4-dependent manner. COX2 is critical for the secretion of prostaglandin E2 and was strongly induced by H2O2 or TNFα only in presence of NRF2. Induction of MITF and depletion of COX2 and PGE2 were also observed in NRF2-deleted melanoma cells in vivo. Furthermore, genes corresponding to the innate immune response such as RSAD2 and IFIH1 were strongly elevated in absence of NRF2 and coincided with immune evasion parameters in human melanoma datasets. Even in vitro, NRF2 activation or prostaglandin E2 supplementation blunted the induction of the innate immune response in melanoma cells. Transcriptome analyses from lung adenocarcinomas indicate that the observed link between NRF2 and the innate immune response is not restricted to melanoma.

scholarly journals Leptospira interrogans Catalase Is Required for Resistance to H2O2and for Virulence

2012 ◽  
Vol 80 (11) ◽  
pp. 3892-3899 ◽  
Author(s):  
Azad Eshghi ◽  
Kristel Lourdault ◽  
Gerald L. Murray ◽  
Thanatchaporn Bartpho ◽  
Rasana W. Sermswan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Immune Response ◽  
Innate Immune Response ◽  
Reactive Oxygen ◽  
Innate Immune ◽  
Leptospira Interrogans ◽  
Oxygen Species ◽  
Content Type ◽  
Host Innate Immune Response

ABSTRACTPathogenicLeptospiraspp. are likely to encounter higher concentrations of reactive oxygen species induced by the host innate immune response. In this study, we characterizedLeptospira interroganscatalase (KatE), the only annotated catalase found within pathogenicLeptospiraspecies, by assessing its role in resistance to H2O2-induced oxidative stress and during infection in hamsters. PathogenicL. interrogansbacteria had a 50-fold-higher survival rate under H2O2-induced oxidative stress than did saprophyticL. biflexabacteria, and this was predominantly catalase dependent. We also characterized KatE, the only annotated catalase found within pathogenicLeptospiraspecies. Catalase assays performed with recombinant KatE confirmed specific catalase activity, while protein fractionation experiments localized KatE to the bacterial periplasmic space. The insertional inactivation ofkatEin pathogenicLeptospirabacteria drastically diminished leptospiral viability in the presence of extracellular H2O2and reduced virulence in an acute-infection model. Combined, these results suggest thatL. interrogansKatE confersin vivoresistance to reactive oxygen species induced by the host innate immune response.

scholarly journals The impact of vitamin D on the innate immune response to uropathogenic Escherichia coli during pregnancy

2015 ◽  
Vol 21 (5) ◽  
pp. 482.e1-482.e7 ◽  
Author(s):  
N.L. Ramos ◽  
M. Sekikubo ◽  
F. Kironde ◽  
F. Mirembe ◽  
M. Sääf ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Vitamin D ◽  
Immune Response ◽  
Innate Immune Response ◽  
Uropathogenic Escherichia Coli ◽  
Innate Immune ◽  
The Impact

scholarly journals 1-Trichloromethyl-1,2,3,4-tetrahydro-beta-carboline (TaClo) Induces the Apoptosis of Dopaminergic Neurons via Oxidative Stress and Neuroinflammation

2019 ◽  
Vol 2019 ◽  
pp. 1-12 ◽  
Author(s):  
Yihang Yang ◽  
Bo Pang ◽  
Zihao Liu ◽  
Jie Li ◽  
Zhen Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Immune Response ◽  
Innate Immune Response ◽  
Diffusion Tensor ◽  
Underlying Mechanism ◽  
Innate Immune ◽  
Motor Dysfunction ◽  
Mass Spectrometry Analysis ◽  
Nigrostriatal System

Several in vitro studies have revealed the neurotoxicity of 1-trichloromethyl-1,2,3,4-tetrahydro-beta-carboline (TaClo). However, the underlying mechanism has not been completely elucidated, particularly in vivo. This study was designed to study the neurotoxicity of TaClo in vivo by stereotactically injecting TaClo into the striatum of Wistar rats. After the TaClo injections, rats were subjected to an open field test, and their distance travelled and tracks showed decreasing trends over time. The results of liquid chromatography-mass spectrometry analysis showed that the motor dysfunction of the TaClo-treated rats was accompanied by reduced dopamine levels in the striatum. Based on the diffusion tensor imaging data, the apparent diffusion coefficient of the nigrostriatal pathway was significantly increased, and subsequent histological staining revealed the demyelination of nigrostriatal fibres after the TaClo treatment. TaClo induced a loss of tyrosine hydroxylase-positive cells in the substantia nigra compacta. Regarding the underlying mechanism, TaClo caused oxidative stress in the nigrostriatal system by increasing the production of reactive oxygen species and reducing the mitochondria membrane potential. Meanwhile, the elevated expression of Iba-1, TNF-α, IL-6, Cox-2, and iNOS indicated microglial activation and a strong innate immune response in the nigrostriatal system. In addition, activated caspase-3 levels were increased. Thus, both mitochondrial impairments and the innate immune response are involved in TaClo-induced neurotoxicity.

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