Pregnancy, indoleamine 2,3-dioxygenase (IDO) and chlamydial abortion: an unresolved paradox

Gary Entrican, Sean Wattegedera, Mara Rocchi, Nicholas Wheelhouse

Research output: Contribution to journalArticlepeer-review


Chlamydophila abortus infects the placental trophoblast in sheep, humans and mice, causing cell damage and inflammation that culminates in abortion. Host control of C. abortus appears to be heavily dependant on interferon (IFN)-gamma production. IFN-gamma induces expression of the enzyme indoleamine 2,3-dioxygenase (IDO), resulting in the degradation of intracellular pools of tryptophan, thereby depriving the organism of this essential growth nutrient. The anti-chlamydial effects of IFN-gamma can be reversed by the addition of exogenous tryptophan. This finding is consistent with studies of the C. abortus genome sequence that have revealed that the organism lacks the capability to synthesise tryptophan from host cell substrates and is therefore dependant on host tryptophan. This raises an interesting paradox since the placental trophoblast in humans and mice is known to constitutively express IDO and degrade tryptophan, a phenomenon that has been linked to maternal immunological tolerance of the semi-allogeneic fetus. This paradox is discussed in the context of immune modulation during pregnancy, tryptophan biosynthesis by Chlamydiaceae and differences in placental structures between sheep, humans and mice.
Original languageEnglish
Pages (from-to)98-102
Number of pages5
JournalVeterinary Microbiology
Issue number1-2
Publication statusPublished - 16 Mar 2009


  • Abortion, Spontaneous
  • Animals
  • Chlamydophila Infections
  • Female
  • Gene Expression Regulation, Enzymologic
  • Humans
  • Indoleamine-Pyrrole 2,3,-Dioxygenase
  • Interferon-gamma
  • Mice
  • Pregnancy
  • Sheep
  • Sheep Diseases
  • Tryptophan

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