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Type I interferons regulate susceptibility to inflammation-induced preterm birth

Monica Cappelletti1, Pietro Presicce2, Matthew J Lawson1,3

  • 1Division of Immunobiology.

JCI Insight
|March 15, 2017
PubMed

Insights

Type I interferons (IFN) and their receptor (IFNAR) activation can trigger inflammation, leading to preterm birth (PTB). This pathway, conserved across species, offers a potential biomarker and therapeutic target for preventing PTB.

Area of Science:

  • Immunology
  • Reproductive Biology
  • Infectious Disease

Background:

  • Preterm birth (PTB) is a major global cause of infant mortality.
  • Maternal inflammation, often from microbial infections, is a key risk factor for PTB.
  • The mechanisms by which pathogens induce PTB or enhance susceptibility to secondary infections are not fully understood.

Purpose of the Study:

  • To investigate the role of type I interferon (IFN) signaling in pathogen-induced preterm birth.
  • To identify biological pathways linking pathogen-associated molecular patterns to PTB.
  • To explore the potential of the type I IFN/IFN receptor (IFNAR) axis as a therapeutic target for PTB.

Main Methods:

  • Utilized mouse models to study the effects of pathogen-associated molecular patterns and recombinant type I IFNs on PTB.
  • Assessed the impact of genetic deficiencies in type I IFN, Toll-like receptor (TLR), and IL-6 signaling on PTB induction.
  • Examined the role of hematopoietic cell type I IFNAR signaling in regulating cytokine production.
  • Analyzed type I IFN and cytokine expression in human PTB cases.

Main Results:

  • Activation of the type I IFN/IFNAR pathway by pathogens or their components primes for systemic and uterine inflammation, leading to PTB.
  • Recombinant type I IFNs exacerbated inflammation and reduced the threshold for PTB induction.
  • Impaired type I IFN, TLR, or IL-6 responsiveness abrogated inflammatory challenge-induced PTB.
  • Type I IFN sensing by IFNAR on hematopoietic cells is crucial for regulating inflammatory cytokine production.
  • Type I IFN priming effects and elevated type I IFN/cytokine expression are observed in human PTB.

Conclusions:

  • The type I IFN/IFNAR axis plays a critical role in priming the inflammatory cascade that leads to preterm birth.
  • This pathway is conserved across species, including humans.
  • Targeting the type I IFN/IFNAR axis presents a promising strategy for developing biomarkers and therapeutics to prevent PTB.

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