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  • 1
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    Conjugated action of two species-specific invasion proteins for fetoplacental listeriosis (2008)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2008-09-23
    Description: The ability to cross host barriers is an essential virulence determinant of invasive microbial pathogens. Listeria monocytogenes is a model microorganism that crosses human intestinal and placental barriers, and causes severe maternofetal infections by an unknown mechanism. Several studies have helped to characterize the bacterial invasion proteins InlA and InlB. However, their respective species specificity has complicated investigations on their in vivo role. Here we describe two novel and complementary animal models for human listeriosis: the gerbil, a natural host for L. monocytogenes, and a knock-in mouse line ubiquitously expressing humanized E-cadherin. Using these two models, we uncover the essential and interdependent roles of InlA and InlB in fetoplacental listeriosis, and thereby decipher the molecular mechanism underlying the ability of a microbe to target and cross the placental barrier.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Disson, Olivier -- Grayo, Solene -- Huillet, Eugenie -- Nikitas, Georgios -- Langa-Vives, Francina -- Dussurget, Olivier -- Ragon, Marie -- Le Monnier, Alban -- Babinet, Charles -- Cossart, Pascale -- Lecuit, Marc -- Howard Hughes Medical Institute/ -- England -- Nature. 2008 Oct 23;455(7216):1114-8. doi: 10.1038/nature07303. Epub 2008 Sep 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut Pasteur, Groupe Microorganismes et Barrieres de l'Hote, Unite des Interactions Bacteries-Cellules, F-75015 Paris, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18806773" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacterial Proteins/genetics/*metabolism ; Cadherins/genetics ; Cells, Cultured ; Disease Models, Animal ; Enterocytes/microbiology ; Epithelial Cells/microbiology ; Female ; Fetal Diseases/*microbiology ; Gerbillinae ; Humans ; Listeria monocytogenes/*physiology ; Listeriosis/microbiology/*transmission ; *Maternal-Fetal Exchange ; Membrane Proteins/genetics/*metabolism ; Mice ; Molecular Sequence Data ; Placenta Diseases/*microbiology ; Pregnancy ; Pregnancy Complications, Infectious/metabolism/microbiology ; Protein Binding ; Receptors, Growth Factor/metabolism ; Species Specificity
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 2
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    IFITM proteins inhibit placental syncytiotrophoblast formation and promote fetal demise (2019)
    American Association for the Advancement of Science (AAAS)
    In: Science
    Details
    Publication Date: 2019
    Description: 〈p〉Elevated levels of type I interferon (IFN) during pregnancy are associated with intrauterine growth retardation, preterm birth, and fetal demise through mechanisms that are not well understood. A critical step of placental development is the fusion of trophoblast cells into a multinucleated syncytiotrophoblast (ST) layer. Fusion is mediated by syncytins, proteins deriving from ancestral endogenous retroviral envelopes. Using cultures of human trophoblasts or mouse cells, we show that IFN-induced transmembrane proteins (IFITMs), a family of restriction factors blocking the entry step of many viruses, impair ST formation and inhibit syncytin-mediated fusion. Moreover, the IFN inducer polyinosinic:polycytidylic acid promotes fetal resorption and placental abnormalities in wild-type but not in 〈i〉Ifitm-〈/i〉deleted mice. Thus, excessive levels of IFITMs may mediate the pregnancy complications observed during congenital infections and other IFN-induced pathologies.〈/p〉
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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