Decreased tryptophan catabolism by placental indoleamine 2,3-dioxygenase in preeclampsia

Kudo, Yoshiki; Boyd, C. A. R.; Sargent, Ian L.; Redman, Christopher W.G.

doi:10.1067/mob.2003.156

Cited by 100 publications

(96 citation statements)

References 29 publications

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“…In preeclampsia, placental tryptophan-degrading activity and placental IDO1 mRNA are reduced [44]. A lower level of IDO immunostaining in placental villi has been reported [45].…”

Section: Expression Of Ido1 In the Human Placentamentioning

confidence: 95%

Expression von Indolamin 2,3-dioxygenase in der Plazenta

Sedlmayr

Blaschitz

2012

Wien Med Wochenschr

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“…In preeclampsia, placental tryptophan-degrading activity and placental IDO1 mRNA are reduced [44]. A lower level of IDO immunostaining in placental villi has been reported [45].…”

Section: Expression Of Ido1 In the Human Placentamentioning

confidence: 95%

Expression von Indolamin 2,3-dioxygenase in der Plazenta

Sedlmayr

Blaschitz

2012

Wien Med Wochenschr

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“…Indirect measures suggest that IDO is less active in stage 3 pre-eclampsia. 61 Given that 3rd stage pre-eclampsia involves maternal systemic inflammation, it would be predicted that IDO would be activated. So this observation is unexplained.…”

Section: Immunoregulation In Stage 3 Pre-eclampsiamentioning

confidence: 99%

REVIEW ARTICLE: Immunology of Pre‐Eclampsia

Redman

Sargent

2010

American J Rep Immunol

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606

486

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Citation Redman CWG, Sargent IL. Immunology of Pre‐eclampsia. Am J Reprod Immunol 2010Pre‐eclampsia develops in stages, only the last being the clinical illness. This is generated by a non‐specific, systemic (vascular), inflammatory response, secondary to placental oxidative stress and not by reactivity to fetal alloantigens. However, maternal adaptation to fetal (paternal alloantigens) is crucial in the earlier stages. A pre‐conceptual phase involves maternal tolerization to paternal antigens by seminal plasma. After conception, regulatory T cells, interacting with indoleamine 2,3‐dioxygenase, together with decidual NK cell recognition of fetal HLA‐C on extravillous trophoblast may facilitate placental growth by immunoregulation. Complete failure of this mechanism would cause miscarriage, while partial failure would cause poor placentation and dysfunctional uteroplacental perfusion. The first pregnancy preponderance and partner specificity of pre‐eclampsia can be explained by this model. For the first time, the pathogenesis of pre‐eclampsia can be related to defined immune mechanisms that are appropriate to the fetomaternal frontier. Now, the challenge is to prove the detail.

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“…This also supports Nishizawa and colleagues' hypothesis that decreased IDO activity may increase oxidative stress in the pre-eclamptic placenta. Others have shown that kynurenine: tryptophan ratios are increased in normotensive pregnant women but not in pre-eclamptic women [Kudo et al 2003]. Still others have confirmed immunohistologically that IDO levels are lower in pre-eclamptic placentas when compared to controls [Santoso et al 2002].…”

mentioning

confidence: 79%

“…Several authors have argued that oxidative stress is central to the pathogenesis of pre-eclampsia, particularly early-onset disease [Burton 2009;Kudo et al 2003;Redman and Sargent 2009;Roberts and Hubel 2009]. Much of this hypothesis is based on a series of elegant experiments by Burton and Jauniaux [2004] showing that the human fetus typically develops in an environment that is quite hypoxic.…”

mentioning

confidence: 99%