IFITM1 inhibits trophoblast invasion and is induced in placentas associated with IFN-mediated pregnancy diseases

Degrelle, Séverine A.; Buchrieser, Julian; Dupressoír, Anne; Porrot, Françoise; Lœuillet, Laurence; Fournier, Thierry

doi:10.1016/j.isci.2023.107147

Cited by 5 publications

(2 citation statements)

References 45 publications

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“…145 Moreover, CMV infection dampens EVT invasion [146][147][148][149] by reducing the expression of matrix metalloproteinases, 150 enzymes used by EVT to migrate into the decidua, 151 and dysregulation of the cell matrix and cell-to-cell adhesion molecules. 152 These experimental findings are supported by other studies showing that IFITM1 expression is increased in the EVT and STB of CMV-positive placentas, 64 and CMV suppresses the syncytialization of primary CTB, resulting in reduced PlGF secretion. 153 In addition, CMV-infected decidual fibroblasts alter the phenotype of decidual NK cells from angiogenic to cytotoxic.…”

Section: Cytomegalovirussupporting

confidence: 75%

“…62 IFN-β, a key antiviral cytokine produced in response to infectious pathogens, and particularly viruses, 63 induce the expression of interferon-induced transmembrane proteins (IFITMs) on EVT, which reduces their invasion in vitro. 64 Conversely, another in vitro study demonstrated that ssRNA facilitates EVT migration, 65 implying virus-type specific responses.…”

Section: Poor Placentationmentioning

confidence: 99%

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Implication of viruses in the etiology of preeclampsia

Motomura,

Morita,

Naruse

et al. 2024

American J Rep Immunol

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Preeclampsia is one of the most common disorders that poses threat to both mothers and neonates and a major contributor to perinatal morbidity and mortality worldwide. Viral infection during pregnancy is not typically considered to cause preeclampsia; however, syndromic nature of preeclampsia etiology and the immunomodulatory effects of viral infections suggest that microbes could trigger a subset of preeclampsia. Notably, SARS‐CoV‐2 infection is associated with an increased risk of preeclampsia. Herein, we review the potential role of viral infections in this great obstetrical syndrome. According to in vitro and in vivo experimental studies, viral infections can cause preeclampsia by introducing poor placentation, syncytiotrophoblast stress, and/or maternal systemic inflammation, which are all known to play a critical role in the development of preeclampsia. Moreover, clinical and experimental investigations have suggested a link between several viruses and the onset of preeclampsia via multiple pathways. However, the results of experimental and clinical research are not always consistent. Therefore, future studies should investigate the causal link between viral infections and preeclampsia to elucidate the mechanism behind this relationship and the etiology of preeclampsia itself.

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Section: Cytomegalovirussupporting

confidence: 75%

Section: Poor Placentationmentioning

confidence: 99%

Implication of viruses in the etiology of preeclampsia

Motomura,

Morita,

Naruse

et al. 2024

American J Rep Immunol

View full text Add to dashboard Cite

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Nucleotide metabolism, leukodystrophies, and CNS pathology

Gavazzi,

Gonzalez,

Arnold

et al. 2024

J of Inher Metab Disea

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The balance between a protective and a destructive immune response can be precarious, as exemplified by inborn errors in nucleotide metabolism. This class of inherited disorders, which mimics infection, can result in systemic injury and severe neurologic outcomes. The most common of these disorders is Aicardi Goutières syndrome (AGS). AGS results in a phenotype similar to “TORCH” infections (Toxoplasma gondii, Other [Zika virus (ZIKV), human immunodeficiency virus (HIV)], Rubella virus, human Cytomegalovirus [HCMV], and Herpesviruses), but with sustained inflammation and ongoing potential for complications. AGS was first described in the early 1980s as familial clusters of “TORCH” infections, with severe neurology impairment, microcephaly, and basal ganglia calcifications (Aicardi & Goutières, Ann Neurol, 1984;15:49–54) and was associated with chronic cerebrospinal fluid (CSF) lymphocytosis and elevated type I interferon levels (Goutières et al., Ann Neurol, 1998;44:900–907). Since its first description, the clinical spectrum of AGS has dramatically expanded from the initial cohorts of children with severe impairment to including individuals with average intelligence and mild spastic paraparesis. This broad spectrum of potential clinical manifestations can result in a delayed diagnosis, which families cite as a major stressor. Additionally, a timely diagnosis is increasingly critical with emerging therapies targeting the interferon signaling pathway. Despite the many gains in understanding about AGS, there are still many gaps in our understanding of the cell‐type drivers of pathology and characterization of modifying variables that influence clinical outcomes and achievement of timely diagnosis.

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