Mitochondrial dynamics and the innate antiviral immune response

Pourcelot, Marie; Arnoult, Damien

doi:10.1111/febs.12940

Cited by 43 publications

(42 citation statements)

References 92 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The surviving fraction at each dose was calculated with respect to the plating efficiency of the non-irradiated control. The survival curves were fitted to a linear-quadratic model: SF=exp (-αD-βD 2 ), where SF is the surviving fraction and D is the physical dose, by data analysis software Origin Pro 9.0J (OriginLab Co., Northampton, MA, USA).…”

Section: Reagentsmentioning

confidence: 99%

See 1 more Smart Citation

Effects of retinoic acid-inducible gene-I-like receptors activations and ionizing radiation cotreatment on cytotoxicity against human non-small cell lung cancer inï¿½vitro

et al. 2018

View full text Add to dashboard Cite

Abstract. Retinoic acid-inducible gene-I (RIG-I)-like receptors (RLRs) are pattern-recognition receptors that recognize pathogen-associated molecular patterns and induce antiviral immune responses. Recent studies have demonstrated that RLR activation induces antitumor immunity and cytotoxicity against different types of cancer, including lung cancer. However a previous report has demonstrated that ionizing radiation exerts a limited effect on RLR in human monocytic cell-derived macrophages, suggesting that RLR agonists may be used as effective immunostimulants during radiation therapy. However, it is unclear whether ionizing radiation affects the cytotoxicity of RLR agonists against cancer cells. Therefore, in the present study the effects of cotreatment with ionizing radiation and RLR agonists on cytotoxicity against human non-small cell lung cancer cells A549 and H1299 was investigated. Treatment with RLR agonist poly(I:C)/LyoVec™ [poly(I:C)] exerted cytotoxic effects against human non-small cell lung cancer. The cytotoxic effects of poly(I:C) were enhanced by cotreatment with ionizing radiation, and poly(I:C) pretreatment resulted in the radiosensitization of non-small cell lung cancer. Furthermore, cotreatment of A549 and H1299 cells with poly(I:C) and ionizing radiation effectively induced apoptosis in a caspase-dependent manner compared with treatment with poly(I:C) or ionizing radiation alone. These results indicate that RLR agonists and ionizing radiation cotreatment effectively exert cytotoxic effects against human non-small cell lung cancer through caspase-mediated apoptosis.

show abstract

Section: Reagentsmentioning

confidence: 99%

“…In addition, a recent study showed that mitochondria are involved in innate immune response to RNA viruses (2).…”

Section: Introductionmentioning

confidence: 99%

Effects of retinoic acid-inducible gene-I-like receptors activations and ionizing radiation cotreatment on cytotoxicity against human non-small cell lung cancer inï¿½vitro

et al. 2018

View full text Add to dashboard Cite

show abstract

“…851 Once activated, these proteins interact with mitochondrial anti-viral 852 signaling protein (MAVS), which inserts its caspase activation and 853 recruitment domain (CARD) into the outer mitochondrial membrane.854This causes a signaling cascade that activates proteins of the innate 855 immune system[161]. During infection, there is an increased associa-856 tion of the endoplasmic reticulum with mitochondria, particularly 857 elongated mitochondria.…”

mentioning

confidence: 99%

The role of mitochondrial dysfunction in age-related diseases

Lane¹,

Hilsabeck²,

Rea

2015

Biochimica et Biophysica Acta (BBA) - Bioenergetics

179

142

View full text Add to dashboard Cite

The aging process is accompanied by the onset of disease and a general decline in wellness. Insights into the aging process have revealed a number of cellular hallmarks of aging, among these epigenetic alterations, loss of proteostasis, mitochondrial dysfunction, cellular senescence, and stem cell exhaustion. Mitochondrial dysfunction increasingly appears to be a common factor connecting several of these hallmarks, driving the aging process and afflicting tissues throughout the body. Recent research has uncovered a much more complex involvement of mitochondria in the cell than has previously been appreciated and revealed novel ways in which mitochondrial defects feed into disease pathology. In this review we evaluate ways in which problems in mitochondria contribute to disease beyond the well-known mechanisms of oxidative stress and bioenergetic deficits, and we predict the direction that mitochondrial disease research will take in years to come.

show abstract

“…This interconnection is particularly obvious for MAVS-mediated innate antiviral pathways or for programmed cell death induction [9]. In any case, the main function of the mitochondrion is to orchestrate the production of ATP in the cell.…”

Section: Discussionmentioning

confidence: 99%

“…Indeed, mitochondrion plays the role of a docking station for the multiprotein complex leading to their activation. Beyond its role of adaptor of the antiviral signaling, the mitochondrion is the organelle orchestrating the defense of the infected cell thanks to its critical role in apoptosis and its capacity to produce reactive oxygen species (ROS) [9]. Alongside these immune pathways, cells can react to a sudden increase of extracellular ATP, which is considered a danger signal, through the activation of the purinergic receptor P2X7 [10].…”

Section: Introductionmentioning

confidence: 99%

Transcriptomic profiling of a chicken lung epithelial cell line (CLEC213) reveals a mitochondrial respiratory chain activity boost during influenza virus infection

et al. 2017

View full text Add to dashboard Cite

Avian Influenza virus (AIV) is a major concern for the global poultry industry. Since 2012, several countries have reported AIV outbreaks among domestic poultry. These outbreaks had tremendous impact on poultry production and socio-economic repercussion on farmers. In addition, the constant emergence of highly pathogenic AIV also poses a significant risk to human health. In this study, we used a chicken lung epithelial cell line (CLEC213) to gain a better understanding of the molecular consequences of low pathogenic AIV infection in their natural host. Using a transcriptome profiling approach based on microarrays, we identified a cluster of mitochondrial genes highly induced during the infection. Interestingly, most of the regulated genes are encoded by the mitochondrial genome and are involved in the oxidative phosphorylation metabolic pathway. The biological consequences of this transcriptomic induction result in a 2.5- to 4-fold increase of the ATP concentration within the infected cells. PB1-F2, a viral protein that targets the mitochondria was not found associated to the boost of activity of the respiratory chain. We next explored the possibility that ATP may act as a host-derived danger signal (through production of extracellular ATP) or as a boost to increase AIV replication. We observed that, despite the activation of the P2X7 purinergic receptor pathway, a 1mM ATP addition in the cell culture medium had no effect on the virus replication in our epithelial cell model. Finally, we found that oligomycin, a drug that inhibits the oxidative phosphorylation process, drastically reduced the AIV replication in CLEC213 cells, without apparent cellular toxicity. Collectively, our results suggest that AIV is able to boost the metabolic capacities of its avian host in order to provide the important energy needs required to produce progeny virus.

show abstract

Mitochondrial dynamics and the innate antiviral immune response

Cited by 43 publications

References 92 publications

Effects of retinoic acid-inducible gene-I-like receptors activations and ionizing radiation cotreatment on cytotoxicity against human non-small cell lung cancer inï¿½vitro

Effects of retinoic acid-inducible gene-I-like receptors activations and ionizing radiation cotreatment on cytotoxicity against human non-small cell lung cancer inï¿½vitro

The role of mitochondrial dysfunction in age-related diseases

Transcriptomic profiling of a chicken lung epithelial cell line (CLEC213) reveals a mitochondrial respiratory chain activity boost during influenza virus infection

Contact Info

Product

Resources

About