Fulvia Milena Cribiù

Dr. Fulvia Milena Cribiù

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Research Focus & Metrics

Academic Career Length

9Years (2018-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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15 March 2021 in Journal of Clinical Investigation
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Journal Article
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FCFulvia Milena Cribiù
Fulvia Milena Cribiù
RERoberta Erra
Roberta Erra
LPLorenza Pugni
Lorenza Pugni
CRCarlota Rubio-Perez
Carlota Rubio-Perez
LALidia Alonso
Lidia Alonso
Paolo NuciforoPaolo Nuciforo
Paolo Nuciforo
The effect of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection on the pathophysiology of the placenta and its impact on pregnancy outcome has not yet been fully elucidated. Here, we present a comprehensive clinical, morphological, and molecular analysis of placental tissues from pregnant women with and without SARS-CoV-2 infection. SARS-CoV-2 could be detected in half of placental tissues from SARS-CoV-2–positive women. The presence of the virus was not associated with any distinctive pathological, maternal, or neonatal outcome features. SARS-CoV-2 tissue load was low in all but one patient who exhibited severe placental damage leading to neonatal neurological manifestations. The placental transcriptional response induced by high viral load of SARS-CoV-2 showed an immunopathology phenotype similar to autopsy lung tissues from patients with severe coronavirus disease 2019. This finding contrasted with the lack of inflammatory response in placental tissues from SARS-CoV-2–positive women with low viral tissue load and from SARS-CoV-2–negative women. Importantly, no evidence of vertical transmission of SARS-CoV-2 was found in any newborns, suggesting that the placenta may be an effective maternal-neonatal barrier against the virus even in the presence of severe infection. Our observations suggest that severe placental damage induced by the virus may be detrimental for the neonate independently of vertical transmission.

28 May 2019 in Cells
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Journal Article
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CBClaudia Burrello
Claudia Burrello
MGMaria Rita Giuffrè
Maria Rita Giuffrè
AMAngeli Dominique Macandog
Angeli Dominique Macandog
ADAngelica Diaz-Basabe
Angelica Diaz-Basabe
FCFulvia Milena Cribiù
Fulvia Milena Cribiù
FFFederica Facciotti
Federica Facciotti
Different gastrointestinal disorders, including inflammatory bowel diseases (IBD), have been linked to alterations of the gut microbiota composition, namely dysbiosis. Fecal microbiota transplantation (FMT) is considered an encouraging therapeutic approach for ulcerative colitis patients, mostly as a consequence of normobiosis restoration. We recently showed that therapeutic effects of FMT during acute experimental colitis are linked to functional modulation of the mucosal immune system and of the gut microbiota composition. Here we analysed the effects of therapeutic FMT administration during chronic experimental colitis, a condition more similar to that of IBD patients, on immune-mediated mucosal inflammatory pathways. Mucus and feces from normobiotic donors were orally administered to mice with established chronic Dextran Sodium Sulphate (DSS)-induced colitis. Immunophenotypes and functions of infiltrating colonic immune cells were evaluated by cytofluorimetric analysis. Compositional differences in the intestinal microbiome were analyzed by 16S rRNA sequencing. Therapeutic FMT in mice undergoing chronic intestinal inflammation was capable to decrease colonic inflammation by modulating the expression of pro-inflammatory genes, antimicrobial peptides, and mucins. Innate and adaptive mucosal immune cells manifested a reduced pro-inflammatory profile in FMT-treated mice. Finally, restoration of a normobiotic core ecology contributed to the resolution of inflammation. Thus, FMT is capable of controlling chronic intestinal experimental colitis by inducing a concerted activation of anti-inflammatory immune pathways, mechanistically supporting the positive results of FMT treatment reported in ulcerative colitis patients.

1 August 2018 in Best Practice & Research Clinical Obstetrics & Gynaecology
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Journal Article
Closed access
PVPaolo Pietro Vercellini
Paolo Pietro Vercellini
Paola Vigano'Paola Vigano'
Paola Vigano'
Laura BuggioLaura Buggio
Laura Buggio
SMSofia Makieva
Sofia Makieva
GSGiovanna Scarfone
Giovanna Scarfone
ESEdgardo Somigliana
Edgardo Somigliana

18 May 2020 in Cancers
Verified
Journal Article
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HBHadas Bar-Joseph
Hadas Bar-Joseph
Fedro Alessandro Alessandro PeccatoriFedro Alessandro Alessandro Peccatori
Fedro Alessandro Alessandro Peccatori
IBIrit Ben-Aharon
Irit Ben-Aharon
FCFulvia Milena Cribiù
Fulvia Milena Cribiù
GSGiovanna Scarfone
Giovanna Scarfone
Irit Ben-AharonIrit Ben-Aharon
Irit Ben-Aharon
Breast cancer is diagnosed in ~0.3% of pregnant women. Studies that have addressed gestational and neonatal outcomes of chemotherapy during pregnancy have demonstrated increased gestational complications including preeclampsia and intrauterine growth retardation. We hypothesized that anthracycline-induced gestational complications could be derived from direct toxicity on the placenta vasculature. Pregnant ICR mice (day E12.5) were treated with doxorubicin (DXR; 8 mg/kg) or saline, while their umbilical cord blood flow was imaged by pulse-wave (PW) Doppler. Mice were euthanized on day E18.5, and their embryos and placentae were collected for further analysis. Unlike control mice, the DXR-treated mice presented an acute change in the umbilical cord’s blood flow parameters (velocity time integral and heart rate interval), reduced embryos’ weight, reduced placenta efficiency, and modulation in vascular-related pathways of treated placenta proteomics. Apoptosis and proliferation were also enhanced, as demonstrated by TUNEL and proliferating cell nuclear antigen (PCNA) analysis. We further examined the placentae of patients treated with epirubicin (EPI), who had been diagnosed with breast cancer during pregnancy (weeks 27–35). The immunohistochemistry of the EPI-treated human placentae showed enhanced proliferation and apoptosis as compared with matched chemo-naïve placentae, as well as reduced neovascularization (CD34). Our findings suggest that anthracycline-induced vascular insult promotes placental toxicity, and could point to potential agents designated to offset the damage and to reduce gestational complications in pregnant cancer patients.

24 July 2020 in Genes
Verified
Journal Article
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GLGianluca Lopez
Gianluca Lopez
GLGiulia Lazzeri
Giulia Lazzeri
ARAlessandra Rappa
Alessandra Rappa
GIGiuseppe Isimbaldi
Giuseppe Isimbaldi
FCFulvia Milena Cribiù
Fulvia Milena Cribiù
Alessio Di FonzoAlessio Di Fonzo
Alessio Di Fonzo
Genetic alterations of leucine-rich repeat kinase 2 (LRRK2), one of the most important contributors to familial Parkinson’s disease (PD), have been hypothesized to play a role in cancer development due to demographical and preclinical data. Here, we sought to define the prevalence and prognostic significance of LRRK2 somatic mutations across all types of human malignancies by querying the publicly available online genomic database cBioPortal. Ninety-six different studies with 14,041 cases were included in the analysis, and 761/14,041 (5.4%) showed genetic alterations in LRRK2. Among these, 585 (76.9%) were point mutations, indels or fusions, 168 (22.1%) were copy number variations (CNVs), and 8 (1.0%) showed both types of alterations. One case showed the somatic mutation R1441C. A significant difference in terms of overall survival (OS) was noted between cases harboring somatic LRRK2 whole deletions, amplifications, and CNV-unaltered cases (median OS: 20.09, 57.40, and 106.57 months, respectively; p = 0.0008). These results suggest that both LRRK2 amplifications and whole gene deletions could play a role in cancer development, paving the way for future research in terms of potential treatment with LRRK2 small molecule inhibitors for LRRK2-amplified cases.