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Human Cervical Mucus Plugs Exhibit Insufficiencies in Antimicrobial Activity Towards Group B Streptococcus

Journal article
Authors J. Vornhagen
P. Quach
V. Santana-Ufret
V. Alishetti
A. Brokaw
B. Armistead
H. Q. Tang
J. W. MacDonald
T. K. Bammler
Kristina M. Adams Waldorf
N. Uldbjerg
L. Rajagopal
Published in Journal of Infectious Diseases
Volume 217
Issue 10
Pages 1626-1636
ISSN 0022-1899
Publication year 2018
Published at Institute of Clinical Sciences, Department of Obstetrics and Gynecology
Pages 1626-1636
Language en
Links https://doi.org/10.1093/infdis/jiy0...
Keywords cervical mucus plugs, antimicrobial peptide, group B streptococcus, growth inhibition, pregnancy, capsular polysaccharide, amniotic cavity, s100 proteins, l-ficolin, infection, preterm, pregnancy, virulence, complement, mechanisms, Immunology, Infectious Diseases, Microbiology
Subject categories Microbiology in the medical area, Infectious Medicine, Immunology

Abstract

Preterm birth is a leading cause of neonatal mortality and lacks an effective therapy. Ascending microbial infections from the lower genital tract lead to infection of the placenta, amniotic fluid, and fetus causing preterm birth or stillbirth. Directly in the path of an ascending infection is the cervical mucus plug (CMP), a dense mucoid structure in the cervical canal with potential antimicrobial properties. In this study, we aimed to define the components of CMP responsible for antimicrobial activity against a common lower genital tract organism associated with preterm birth and stillbirths, namely, group B streptococcus (GBS). Using a quantitative proteomic approach, we identified antimicrobial factors in CMPs that were collected from healthy human pregnancies. However, we noted that the concentration of antimicrobial peptides present in the human CMPs were insufficient to directly kill GBS, and antimicrobial activity, when observed, was due to antibiotics retained in the CMPs. Despite this insufficiency, CMP proteins were able to activate leukocytes in whole blood resulting in increased rates of bacterial killing, suggesting a role for the CMP in enhancing complement-mediated killing or leukocyte activation. This study provides new insight into how the human CMP may limit ascending bacterial infection.

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