Circulating cell-free mitochondrial DNA in pregnancy

Physiology ◽  
2022 ◽  
Author(s):  
Jessica L. Bradshaw ◽  
Spencer C Cushen ◽  
Nicole R Phillips ◽  
Styliani Goulopoulou

Circulating cell-free mitochondrial DNA (ccf-mtDNA) released upon cell injury or death stimulates diverse pattern recognition receptors to activate innate immune responses and initiate systemic inflammation. In this review, we discuss the temporal changes of ccf-mtDNA during pregnancy and its potential contribution to adverse pregnancy outcomes in pregnancy complications.

2015 ◽  
Vol 7 (1) ◽  
pp. 11-16 ◽  
Author(s):  
Chunju Fang ◽  
Xiawei Wei ◽  
Yuquan Wei

2020 ◽  
Vol 48 (6) ◽  
pp. 2823-2838
Author(s):  
Palamou Das ◽  
Oishee Chakrabarti

Mitochondrial DNA (mtDNA) can initiate an innate immune response when mislocalized in a compartment other than the mitochondrial matrix. mtDNA plays significant roles in regulating mitochondrial dynamics as well as mitochondrial unfolded protein response (UPR). The mislocalized extra-mtDNA can elicit innate immune response via cGAS–STING (cyclic GMP-AMP synthase–stimulator of interferon genes) pathway, inducing the expression of the interferon-stimulated genes (ISGs). Also, cytosolic damaged mtDNA is cleared up by various pathways which are responsible for participating in the activation of inflammatory responses. Four pathways of extra-mitochondrial mtDNA clearance are highlighted in this review — the inflammasome activation mechanism, neutrophil extracellular traps formation, recognition by Toll-like receptor 9 and transfer of mtDNA between cells packaged into extracellular vesicles. Anomalies in these pathways are associated with various diseases. We posit our review in the present pandemic situation and discuss how mtDNA elicits innate immune responses against different viruses and bacteria. This review gives a comprehensive picture of the role of extra-mitochondrial mtDNA in infectious diseases and speculates that research towards its understanding would help establish its therapeutic potential.


2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Mikito Shimizu ◽  
Tatsusada Okuno ◽  
Makoto Kinoshita ◽  
Hisae Sumi ◽  
Harutoshi Fujimura ◽  
...  

2010 ◽  
Vol 12 (3) ◽  
pp. 222-230 ◽  
Author(s):  
Kiichi Nakahira ◽  
Jeffrey Adam Haspel ◽  
Vijay A K Rathinam ◽  
Seon-Jin Lee ◽  
Tamas Dolinay ◽  
...  

2015 ◽  
Vol 29 (3) ◽  
pp. 119-129 ◽  
Author(s):  
Richard J. Stevenson ◽  
Deborah Hodgson ◽  
Megan J. Oaten ◽  
Luba Sominsky ◽  
Mehmet Mahmut ◽  
...  

Abstract. Both disgust and disease-related images appear able to induce an innate immune response but it is unclear whether these effects are independent or rely upon a common shared factor (e.g., disgust or disease-related cognitions). In this study we directly compared these two inductions using specifically generated sets of images. One set was disease-related but evoked little disgust, while the other set was disgust evoking but with less disease-relatedness. These two image sets were then compared to a third set, a negative control condition. Using a wholly within-subject design, participants viewed one image set per week, and provided saliva samples, before and after each viewing occasion, which were later analyzed for innate immune markers. We found that both the disease related and disgust images, relative to the negative control images, were not able to generate an innate immune response. However, secondary analyses revealed innate immune responses in participants with greater propensity to feel disgust following exposure to disease-related and disgusting images. These findings suggest that disgust images relatively free of disease-related themes, and disease-related images relatively free of disgust may be suboptimal cues for generating an innate immune response. Not only may this explain why disgust propensity mediates these effects, it may also imply a common pathway.


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