دورية أكاديمية
أعرض في EDS

H1N1 influenza virus infection results in adverse pregnancy outcomes by disrupting tissue-specific hormonal regulation.

التفاصيل البيبلوغرافية
العنوان: H1N1 influenza virus infection results in adverse pregnancy outcomes by disrupting tissue-specific hormonal regulation.
المؤلفون: Littauer EQ; Department of Microbiology & Immunology and Emory Vaccine Center, Emory University School of Medicine, Atlanta, Georgia, United States of America., Esser ES; Department of Microbiology & Immunology and Emory Vaccine Center, Emory University School of Medicine, Atlanta, Georgia, United States of America., Antao OQ; Department of Microbiology & Immunology and Emory Vaccine Center, Emory University School of Medicine, Atlanta, Georgia, United States of America., Vassilieva EV; Department of Microbiology & Immunology and Emory Vaccine Center, Emory University School of Medicine, Atlanta, Georgia, United States of America., Compans RW; Department of Microbiology & Immunology and Emory Vaccine Center, Emory University School of Medicine, Atlanta, Georgia, United States of America., Skountzou I; Department of Microbiology & Immunology and Emory Vaccine Center, Emory University School of Medicine, Atlanta, Georgia, United States of America.
المصدر: PLoS pathogens [PLoS Pathog] 2017 Nov 27; Vol. 13 (11), pp. e1006757. Date of Electronic Publication: 2017 Nov 27 (Print Publication: 2017).
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Public Library of Science Country of Publication: United States NLM ID: 101238921 Publication Model: eCollection Cited Medium: Internet ISSN: 1553-7374 (Electronic) Linking ISSN: 15537366 NLM ISO Abbreviation: PLoS Pathog Subsets: MEDLINE
أسماء مطبوعة: Original Publication: San Francisco, CA : Public Library of Science, c2005-
مواضيع طبية MeSH: Hormones/*metabolism , Influenza A Virus, H1N1 Subtype/*physiology , Influenza, Human/*physiopathology , Pregnancy Complications/*physiopathology, Animals ; Dinoprostone/metabolism ; Female ; Humans ; Influenza, Human/metabolism ; Influenza, Human/mortality ; Influenza, Human/virology ; Lung/metabolism ; Lung/virology ; Male ; Mice ; Mice, Inbred BALB C ; Organ Specificity ; Placenta/metabolism ; Placenta/virology ; Pregnancy ; Pregnancy Complications/metabolism ; Pregnancy Complications/mortality ; Pregnancy Complications/virology ; Pregnancy Outcome ; Progesterone/metabolism
مستخلص: Increased susceptibility to influenza virus infection during pregnancy has been attributed to immunological changes occurring before and during gestation in order to "tolerate" the developing fetus. These systemic changes are most often characterized by a suppression of cell-mediated immunity and elevation of humoral immune responses referred to as the Th1-Th2 shift. However, the underlying mechanisms which increase pregnant mothers' risk following influenza virus infection have not been fully elucidated. We used pregnant BALB/c mice during mid- to late gestation to determine the impact of a sub-lethal infection with A/Brisbane/59/07 H1N1 seasonal influenza virus on completion of gestation. Maternal and fetal health status was closely monitored and compared to infected non-pregnant mice. Severity of infection during pregnancy was correlated with premature rupture of amniotic membranes (PROM), fetal survival and body weight at birth, lung viral load and degree of systemic and tissue inflammation mediated by innate and adaptive immune responses. Here we report that influenza virus infection resulted in dysregulation of inflammatory responses that led to pre-term labor, impairment of fetal growth, increased fetal mortality and maternal morbidity. We observed significant compartment-specific immune responses correlated with changes in hormonal synthesis and regulation. Dysregulation of progesterone, COX-2, PGE2 and PGF2α expression in infected pregnant mice was accompanied by significant remodeling of placental architecture and upregulation of MMP-9 early after infection. Collectively these findings demonstrate the potential of a seasonal influenza virus to initiate a powerful pro-abortive mechanism with adverse outcomes in fetal health.
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معلومات مُعتمدة: HHSN272201400004C United States AI NIAID NIH HHS
المشرفين على المادة: 0 (Hormones)
4G7DS2Q64Y (Progesterone)
K7Q1JQR04M (Dinoprostone)
تواريخ الأحداث: Date Created: 20171128 Date Completed: 20180109 Latest Revision: 20201214
رمز التحديث: 20231215
مُعرف محوري في PubMed: PMC5720832
DOI: 10.1371/journal.ppat.1006757
PMID: 29176767
قاعدة البيانات: MEDLINE
الوصف
تدمد:1553-7374
DOI:10.1371/journal.ppat.1006757