Maternal organic selenium supplementation alleviates LPS induced inflammation, autophagy and ER stress in the thymus and spleen of offspring piglets by improving the expression of selenoproteins

2021 ◽  
Author(s):  
Dajiang Ding ◽  
Daolin Mou ◽  
Lianpeng Zhao ◽  
Xuemei Jiang ◽  
Lianqiang Che ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Immune Response ◽  
T Lymphocytes ◽  
Er Stress ◽  
Innate Immune Response ◽  
Tissue Damage ◽  
Selenium Supplementation ◽  
Innate Immune ◽  
Organic Selenium

Thymus and spleen are the main reservoir for T lymphocytes, which can regulate innate immune response and provides protection against pathogens and tissue damage. Oxidative stress, excessive inflammation, abnormal autophagy...

scholarly journals Mitochondrial UPR negatively regulates wounding-induced innate immune response in C. elegans epidermis

2021 ◽  
Author(s):  
Jianzhi Zhao ◽  
Hongying Fu ◽  
Hengda Zhou ◽  
Xuecong Ren ◽  
Yuanyuan Wang ◽  
...  
Keyword(s):  
Immune Response ◽  
Signaling Pathways ◽  
Innate Immune Response ◽  
Tissue Damage ◽  
P38 Map Kinase ◽  
Innate Immune ◽  
Loss Of Function ◽  
C Elegans ◽  
Unfolded Protein ◽  
Protein Response

Tissue damage elicits a rapid innate immune response that is essential for efficient wound healing and survival of metazoans. It is well known that p38 MAPK kinase, TGF-β, and hemidesmosome signaling pathways have been involved in wounding-induced innate immunity in C. elegans. Here, we find that loss of function of ATFS-1 increased innate immune response while an elevated level of mitochondrial unfolded protein response (mitoUPR) inhibits the innate immune response upon epidermal wounding. Epidermal wounding triggers the nucleus export of ATFS-1 and inhibits themitoUPR in C. elegans epidermis. Moreover, genetic analysis suggests that ATFS-1 functions upstream of the p38 MAP kinase, TGF-β, and DAF-16 signaling pathways in regulating AMPs induction. Thus, our results suggest that the mitoUPR function as an intracellular signal required to fine-tune innate immune response after tissue damage.

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.

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 ER stress and its regulator X-box-binding protein-1 enhance polyIC-induced innate immune response in dendritic cells

2011 ◽  
Vol 41 (4) ◽  
pp. 1086-1097 ◽  
Author(s):  
Fanlei Hu ◽  
Xiaofei Yu ◽  
Hongxia Wang ◽  
Daming Zuo ◽  
Chunqing Guo ◽  
...  
Keyword(s):  
Immune Response ◽  
Dendritic Cells ◽  
Er Stress ◽  
Innate Immune Response ◽  
Binding Protein ◽  
Innate Immune

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.

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