Modulation of the innate immune response, antioxidant system and oxidative stress during acute and chronic stress in pacu (Piaractus mesopotamicus)

Author(s):  
Camila de Fátima Pereira de Faria ◽  
Claudia Bueno dos Reis Martinez ◽  
Leonardo Susumu Takahashi ◽  
Mariana Maluli Marinho de Mello ◽  
Talísia Pereira Martins ◽  
...  
Viruses ◽  
2018 ◽  
Vol 10 (10) ◽  
pp. 540 ◽  
Author(s):  
Sarah Zobel ◽  
Mechthild Lorenz ◽  
Giada Frascaroli ◽  
Janik Böhnke ◽  
Nicole Bilz ◽  
...  

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.


Oncogene ◽  
2020 ◽  
Vol 39 (44) ◽  
pp. 6841-6855 ◽  
Author(s):  
Christina Jessen ◽  
Julia K. C. Kreß ◽  
Apoorva Baluapuri ◽  
Anita Hufnagel ◽  
Werner Schmitz ◽  
...  

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.


Chemosphere ◽  
2018 ◽  
Vol 210 ◽  
pp. 93-101 ◽  
Author(s):  
Jiajing Wei ◽  
Ting Zhou ◽  
Zhiyong Hu ◽  
Ying Li ◽  
Hongfang Yuan ◽  
...  

2012 ◽  
Vol 80 (11) ◽  
pp. 3892-3899 ◽  
Author(s):  
Azad Eshghi ◽  
Kristel Lourdault ◽  
Gerald L. Murray ◽  
Thanatchaporn Bartpho ◽  
Rasana W. Sermswan ◽  
...  

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.


2017 ◽  
Vol 65 ◽  
pp. 96-102 ◽  
Author(s):  
Eduardo Pahor-Filho ◽  
Adriana Soliris Corredor Castillo ◽  
Nycolas Levy Pereira ◽  
Fabiana Pilarski ◽  
Elisabeth Criscuolo Urbinati

2019 ◽  
Vol 2019 ◽  
pp. 1-12 ◽  
Author(s):  
Yihang Yang ◽  
Bo Pang ◽  
Zihao Liu ◽  
Jie Li ◽  
Zhen Zhang ◽  
...  

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.


2021 ◽  
Author(s):  
Dajiang Ding ◽  
Daolin Mou ◽  
Lianpeng Zhao ◽  
Xuemei Jiang ◽  
Lianqiang Che ◽  
...  

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...


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