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Tytuł pozycji:

Matrix Metalloproteinases Expressed in Response to Bacterial Vaginosis Disrupt the Endocervical Epithelium, Increasing Transmigration of HIV.

Tytuł :
Matrix Metalloproteinases Expressed in Response to Bacterial Vaginosis Disrupt the Endocervical Epithelium, Increasing Transmigration of HIV.
Autorzy :
Cherne MD; Laboratory of Innate Host Defense, Burnett School of Biomedical Sciences, College of Medicine, University of Central Florida, Orlando, Florida, USA.
Cole AL; Laboratory of Innate Host Defense, Burnett School of Biomedical Sciences, College of Medicine, University of Central Florida, Orlando, Florida, USA.
Newberry L; Student Health Services, University of Central Florida, Orlando, Florida, USA.
Schmidt-Owens M; Student Health Services, University of Central Florida, Orlando, Florida, USA.
Deichen M; Student Health Services, University of Central Florida, Orlando, Florida, USA.
Cole AM; Laboratory of Innate Host Defense, Burnett School of Biomedical Sciences, College of Medicine, University of Central Florida, Orlando, Florida, USA .
Pokaż więcej
Źródło :
Infection and immunity [Infect Immun] 2020 Mar 23; Vol. 88 (4). Date of Electronic Publication: 2020 Mar 23 (Print Publication: 2020).
Typ publikacji :
Journal Article
Język :
English
Imprint Name(s) :
Publication: Washington, DC : American Society For Microbiology
Original Publication: [Bethesda, Md.] American Society for Microbiology.
MeSH Terms :
Cell Movement*
Permeability*
Endometrium/*pathology
Epithelium/*pathology
Lymphocytes/*physiology
Matrix Metalloproteinases/*metabolism
Vaginosis, Bacterial/*pathology
Cells, Cultured ; Female ; HIV-1/growth & development ; Humans ; Lymphocytes/virology ; Models, Theoretical
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Grant Information :
R21 AI147686 United States AI NIAID NIH HHS
Contributed Indexing :
Keywords: bacterial vaginosis*; female reproductive tract*; human immunodeficiency virus*; matrix metalloproteinases*; mucosal immunity*
Substance Nomenclature :
EC 3.4.24.- (Matrix Metalloproteinases)
Entry Date(s) :
Date Created: 20200226 Date Completed: 20200708 Latest Revision: 20210105
Update Code :
20210209
PubMed Central ID :
PMC7093129
DOI :
10.1128/IAI.00041-20
PMID :
32094253
Czasopismo naukowe
Bacterial vaginosis (BV), a disorder of the female reproductive tract (FRT) in which a healthy Lactobacillus -dominant microflora is replaced by BV-associated bacteria (BVAB), can significantly increase the incidence of human immunodeficiency virus (HIV) acquisition. Discerning the effect of BV on the mucosal epithelium of the FRT may yield novel preventatives and therapeutics for HIV infection. Here, we investigated barrier dysfunction of the endocervix by host-derived factors, secreted in response to BV, as a potential cause of HIV infection. Using a polarized endocervical cell culture system, we determined that conditioned media (CM) from endocervical cells cocultured with BVAB (endocervical+BVAB CM), as well as cervicovaginal fluid (CVF) from women with BV, disrupted epithelial polarization. We assessed host matrix metalloproteinases (MMPs) as the BV-associated secreted factors which disrupt the endocervical epithelium. MMPs were overexpressed in endocervical+BVAB CM and CVF from women with BV and were capable of disrupting endocervical epithelial polarization. When we cocultured polarized endocervical cells with HIV-1-infected lymphocyte-derived cells, we discovered endocervical+BVAB CM and MMPs significantly increased the transmigration of virus through the epithelium, and treatment with an MMP inhibitor decreased these effects. When we examined the effect of CVF on HIV-1 transmigration through endocervical epithelium, we demonstrated that CVF samples with greater concentrations of BV-associated MMPs increased viral transmigration. Our results suggest MMPs increase HIV-1 infection by disrupting the endocervical epithelium, permitting transmigration of virus through the epithelium to infect underlying target cells.
(Copyright © 2020 American Society for Microbiology.)

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