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The determinant role of IL-6 in the establishment of inflammation leading to spontaneous preterm birth

Journal

CYTOKINE & GROWTH FACTOR REVIEWS
Volume 59, Issue -, Pages 118-130

Publisher

ELSEVIER SCI LTD
DOI: 10.1016/j.cytogfr.2020.12.004

Keywords

Interleukin-6; Preterm labor; Preterm birth; Inflammation; Neonatal injuries; Neonatal mortality

Funding

  1. Fonds de Recherche en Sante du Quebec (FRSQ)
  2. Canadian Institutes of Health Research (CIHR)
  3. Mitacs
  4. Natural Sciences and Engineering Research Council of Canada (NSERC)
  5. Programme d'Excellence en Medecine pour l'Initiation En Recherche (PREMIER)
  6. Stollery Children's Hospital Foundation
  7. Lois Hole Hospital for Women through the Women and Children's Health Research Institute

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Preterm birth is a major public health concern due to its association with inflammation, especially IL-6, which plays important roles in the timing of childbirth and fetal tissue damage. Current treatments focus on stopping contractions but do not directly address the maternal inflammation that contributes to premature birth.
Preterm birth (PTB) and its consequences are a major public health concern as preterm delivery is the main cause of mortality and morbidity at birth. There are many causes of PTB, but inflammation is undeniably associated with the process of premature childbirth and fetal injury. At present, treatments clinically available mostly involve attempt to arrest contractions (tocolytics) but do not directly address upstream maternal inflammation on development of the fetus. One of the possible solutions may lie in the modulation of inflammatory mediators. Of the many pro-inflammatory cytokines involved in the induction of PTB, IL-6 stands out for its pleiotropic effects and its involvement in both acute and chronic inflammation. Here, we provide a detailed review of the effects of IL-6 on the timing of childbirth, its occurrence during PTB and its indissociable roles with associated fetal tissue damage.

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