Maternal infection-induced white matter injury is reduced by treatment with interleukin-10

Rodts-Palenik, Sheryl; Wyatt-Ashmead, Josephine; Pang, Yi; Thigpen, Brad; Cai, Zhengwei; Rhodes, Phillip; Martin, James N.; Granger, Joey P.; Bennett, William A.

doi:10.1016/j.ajog.2004.06.093

Cited by 78 publications

(52 citation statements)

References 24 publications

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“…Unfortunately, additional trials and meta-analysis showed that pre-or postnatal corticosteroids eventually do not provide neurobehavioral benefit and could result in adverse effects in certain therapeutic designs (54). Conflicting results and fetal adverse effects such as ductal constriction have been reported in neonates treated prenatally with nonsteroidal anti-inflammatory drugs (55)(56)(57), emphasizing the need to better restrict the target of blocking agents to optimally balance beneficial and adverse effects. Maternal IL-1Ra therapy, as we tested, at doses already recommended for human inflammatory diseases (58) may meet this safety/efficacy criterion.…”

Section: Discussionmentioning

confidence: 99%

IL-1 Receptor Antagonist Protects against Placental and Neurodevelopmental Defects Induced by Maternal Inflammation

Girard

Tremblay

Lepage

et al. 2010

The Journal of Immunology

194

177

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Section: Discussionmentioning

confidence: 99%

IL-1 Receptor Antagonist Protects against Placental and Neurodevelopmental Defects Induced by Maternal Inflammation

Girard

Tremblay

Lepage

et al. 2010

The Journal of Immunology

194

177

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“…IL10 administered either on the day of LPS administration or delayed by 24 hours completely abolished preterm delivery (Terrone et al 2001). Further studies by the same group in a rat E. coli preterm labour model showed that IL10 also prevented infection-induced white matter injury (Rodts-Palenik et al 2004). More recently, Bennett et al have shown that 15-deoxy-12,14-prostaglandin J2 (15d-PGJ2, an agent which inhibits NFKB and possibly also JNK) averts LPS-induced preterm labour in pregnant mice and LPS-induced NFKB activation in the brain of mouse pups (Pirianov et al 2009).…”

Section: Complicated Labourmentioning

confidence: 98%

Inflammatory pathways in female reproductive health and disease

Jabbour¹,

Sales²,

Catalano³

et al. 2009

Reproduction

293

226

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Inflammation involves alterations to vascular and immune cell function. It is well recognised that many physiological reproductive events such as ovulation, menstruation, implantation and onset of labour display hallmark signs of inflammation. These are orchestrated by specific molecular pathways involving a host of growth factors, cytokines, chemokines and lipid mediators. Resumption of normal reproductive function involves prompt and proper resolution of these inflammatory pathways. Recent literature confirms that resolution of inflammatory pathways involves specific biochemical events that are activated to re-establish homeostasis in the affected tissue. Moreover, initiation and maintenance of inflammatory pathways are the key components of many pathologies of the reproductive tract and elsewhere in the body. The onset of reproductive disorders or disease may be the result of exacerbated activation and maintenance of inflammatory pathways or their dysregulated resolution. This review will address the role of inflammatory events in normal reproductive function and its pathologies.

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“…This implies either that LPS is not transported across the placenta and/or that the fetus has alternative mechanisms that block upregulation in TNF-␣ and IL-6 gene expression. Such mechanisms would be expected to be of benefit in sparing the developing fetus from sublethal effects of inflammatory cytokines, particularly the brain which is at risk of intraventricular hemorrhage and white matter damage elicited by endotoxin-induced cytokines during intrauterine infection (30,41). Our findings of differential cytokine content and synthesis in different compartments of the gestational tissues is consistent with a previous report on cytokine production after intrauterine infection in wild-type mice, where considerably more IL-1, IL-6, and TNF-␣ immunoactivity was detected in the uterus than the placenta, and fetal content was lower still (42).…”

Section: Discussionmentioning

confidence: 99%

“…In rats, exogenously administered IL-10 can attenuate fetal loss and growth restriction induced by LPS (28) and abrogate preterm birth and fetal growth impairment elicited by in utero infection with Escherichia coli (29). Furthermore, treatment of rats with IL-10 can reduce the extent of severe fetal brain injury often evident after uterine bacterial infection (30).…”

mentioning

confidence: 99%

Essential Role for IL-10 in Resistance to Lipopolysaccharide-Induced Preterm Labor in Mice

Robertson

Skinner

Care

2006

The Journal of Immunology

174

139

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IL-10 is highly expressed in the uterus and placenta and is implicated in controlling inflammation-induced pathologies of pregnancy. To investigate the role of IL-10 in regulating preterm labor, the response of IL-10 null mutant mice to low-dose LPS in late gestation was evaluated. When IL-10 null mutant C57BL/6 (IL-10−/−) and control (IL-10+/+) mice were administered LPS on day 17 of pregnancy, the dose of LPS required to elicit 50% preterm fetal loss was 10-fold lower in IL-10−/− mice than in IL-10+/+ mice. Surviving fetuses in IL-10−/− mice exhibited fetal growth restriction at lower doses of LPS than IL-10+/+ mice. Marked elevation of LPS-induced immunoactive TNF-α and IL-6 was evident in the serum, uterus, and placenta of IL-10−/− mice, and TNF-α and IL-6 mRNA expression was elevated in the uterus and placenta, but not the fetus. Serum IL-1α, IFN-γ, and IL-12p40 were increased and soluble TNFRII was diminished in the absence of IL-10, with these changes also reflected in the gestational tissues. Administration of rIL-10 to IL-10−/− mice attenuated proinflammatory cytokine synthesis and alleviated their increased susceptibility to preterm loss. Exogenous IL-10 also protected IL-10+/+ mice from fetal loss. These data show that IL-10 modulates resistance to inflammatory stimuli by down-regulating proinflammatory cytokines in the uterus and placenta. Abundance of endogenous IL-10 in gestational tissues is therefore identified as a critical determinant of resistance to preterm labor, and IL-10 may provide a useful therapeutic agent in this common condition.

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Maternal infection-induced white matter injury is reduced by treatment with interleukin-10

Cited by 78 publications

References 24 publications

IL-1 Receptor Antagonist Protects against Placental and Neurodevelopmental Defects Induced by Maternal Inflammation

IL-1 Receptor Antagonist Protects against Placental and Neurodevelopmental Defects Induced by Maternal Inflammation

Inflammatory pathways in female reproductive health and disease

Essential Role for IL-10 in Resistance to Lipopolysaccharide-Induced Preterm Labor in Mice

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