Microbial-driven preterm labour involves crosstalk between the innate and adaptive immune response

Denise Chan, Phillip R. Bennett, Yun S. Lee, Samit Kundu, T. G. Teoh, Malko Adan, Saqa Ahmed, Richard G. Brown, Anna L. David, Holly V. Lewis, Belen Gimeno-Molina, Jane E. Norman, Sarah J. Stock, Vasso Terzidou, Pascale Kropf, Marina Botto, David A. MacIntyre and Lynne Sykes ()
Additional contact information
Denise Chan: Imperial College London
Phillip R. Bennett: Imperial College London
Yun S. Lee: Imperial College London
Samit Kundu: Imperial College London
T. G. Teoh: Imperial College London
Malko Adan: Imperial College London
Saqa Ahmed: Imperial College London
Richard G. Brown: Imperial College London
Anna L. David: University College London
Holly V. Lewis: Imperial College London
Belen Gimeno-Molina: Imperial College London
Jane E. Norman: University of Edinburgh Usher Institute
Sarah J. Stock: University of Edinburgh Usher Institute
Vasso Terzidou: Imperial College London
Pascale Kropf: March of Dimes Prematurity Research Center at Imperial College London
Marina Botto: March of Dimes Prematurity Research Center at Imperial College London
David A. MacIntyre: Imperial College London
Lynne Sykes: Imperial College London

Nature Communications, 2022, vol. 13, issue 1, 1-15

Abstract: Abstract There has been a surge in studies implicating a role of vaginal microbiota in spontaneous preterm birth (sPTB), but most are associative without mechanistic insight. Here we show a comprehensive approach to understand the causative factors of preterm birth, based on the integration of longitudinal vaginal microbiota and cervicovaginal fluid (CVF) immunophenotype data collected from 133 women at high-risk of sPTB. We show that vaginal depletion of Lactobacillus species and high bacterial diversity leads to increased mannose binding lectin (MBL), IgM, IgG, C3b, C5, IL-8, IL-6 and IL-1β and to increased risk of sPTB. Cervical shortening, which often precedes preterm birth, is associated with Lactobacillus iners and elevated levels of IgM, C3b, C5, C5a and IL-6. These data demonstrate a role for the complement system in microbial-driven sPTB and provide a scientific rationale for the development of live biotherapeutics and complement therapeutics to prevent sPTB.

Date: 2022
References: View references in EconPapers View complete reference list from CitEc
Citations: View citations in EconPapers (1)

Downloads: (external link)
https://www.nature.com/articles/s41467-022-28620-1 Abstract (text/html)

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:13:y:2022:i:1:d:10.1038_s41467-022-28620-1

Ordering information: This journal article can be ordered from
https://www.nature.com/ncomms/

DOI: 10.1038/s41467-022-28620-1

Access Statistics for this article

Nature Communications is currently edited by Nathalie Le Bot, Enda Bergin and Fiona Gillespie

More articles in Nature Communications from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().