Models of Fetal Brain Injury, Intrauterine Inflammation, and Preterm Birth

Burd, Irina; Balakrishnan, Bindu; Kannan, Sujatha

doi:10.1111/j.1600-0897.2012.01110.x

Cited by 215 publications

(195 citation statements)

References 69 publications

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“…Reduced neuronal density can also be the end result of neurotoxicity in the central nervous system due to endotoxemia caused by autogenously induced peritonitis and bacterial translocation from the abdominal cavity to the bloodstream [Burd et al, 2012]. Apoptosis may also be involved in this process of brain injury associated with neuronal death [Gavilanes et al, 2009;Kallapur et al, 2014;Lante et al, 2008;Nitsos, Rees, Duncan, Kramer, Harding, Newnham, & Moss, 2006].…”

Section: Discussionmentioning

confidence: 99%

“…In rats, oxidative stress and shortage of glutathione occurred in the fetal brain after maternal lipopolysaccharide administration, and these responses may result in neurodevelopmental deficits in the offspring [Burd, Balakrishnan, & Kannan, 2012].…”

Section: Introductionmentioning

confidence: 99%

“…Such models have resulted in fetal microglial activation, neurotoxicity, and motor and behavioral deficits in the offspring [Burd et al, 2012].…”

Section: Introductionmentioning

confidence: 99%

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Impact of prenatal antimicrobial treatment on fetal brain damage due to autogenous fecal peritonitis in Wistar rats: A Histomorphometric Study

Gadelha¹,

Gadelha

Paz³

et al. 2017

int arch med

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Purpose: To investigate brain neuronal density in newborn rats whose mothers were subjected to fecal peritonitis and compare findings between rats born to mothers treated and not treated with antimicrobials. Methods:Peritonitis was induced with a 10% fecal suspension (4 mL/kg) in 2 pregnant rats. Of these, 1 received antimicrobial treatment 24 hours after peritonitis induction: moxifloxacin and dexamethasone plus 2 mL of the inner bark of the Schinus terebinthifolius raddi extract. One pregnant rat underwent no intervention and served as a control. Results:The newborn brains of rats born to mothers with fecal peritonitis were significantly smaller and of less firm consistency. Brain neuronal density was lower in the untreated group than in the control and treated groups (P < 0.01). Conclusions:Untreated peritonitis caused brain damage in the offspring, which was averted by effective early antimicrobial treatment. This approach may provide an early avenue for translation of such therapy in humans.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Impact of prenatal antimicrobial treatment on fetal brain damage due to autogenous fecal peritonitis in Wistar rats: A Histomorphometric Study

Gadelha¹,

Gadelha

Paz³

et al. 2017

int arch med

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“…Intrauterine infection and inflammation are established risk factors for CP. 35 Obesity is a chronic low-grade inflammatory condition, 36 but it is not clear whether maternal obesity-induced inflammation might have adverse effects on the developing human brain. However, a study in offspring of rats fed a high-fat diet during pregnancy found increased inflammation within the brain at birth.…”

Section: Figurementioning

confidence: 99%

Maternal Prepregnancy BMI and Risk of Cerebral Palsy in Offspring

et al. 2016

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OBJECTIVES: To investigate the association between maternal pre-pregnancy BMI and risk of cerebral palsy (CP) in offspring. METHODS:The study population consisted of 188 788 children in the Mothers and Babies in Norway and Denmark CP study, using data from 2 population-based, prospective birth cohorts: the Norwegian Mother and Child Cohort Study and the Danish National Birth Cohort. Prepregnancy BMI was classified as underweight (BMI <18.5), lower normal weight , upper normal weight ), overweight , and obese (BMI ≥30). CP diagnoses were obtained from the national CP registries. Associations between maternal prepregnancy BMI and CP in offspring were investigated by using logbinomial regression models. RESULTS:The 2 cohorts had 390 eligible cases of CP (2.1 per 1000 live-born children). Compared with mothers in the lower normal weight group, mothers in the upper normal group had a 40% excess risk of having a child with CP (relative risk [RR], 1.35; 95% confidence interval [CI], 1.03-1.78). Excess risk was 60% (RR, 1.56; 95% CI, 1.21-2.01) for overweight mothers and 60% (RR, 1.55; 95% CI 1.11-2.18) for obese mothers. The risk of CP increased ∼4% for each unit increase in BMI (RR, 1.04; 95% CI, 1.02-1.06). Estimates changed little with adjustment for mother's occupational status, age, and smoking habits. CONCLUSIONS:Higher prepregnancy maternal BMI was associated with increased risk of CP in offspring.a Department of Global Public Health and Primary Care, University of Bergen, Bergen, Norway; b Department of Pediatrics, Haukeland University Hospital, Bergen, Norway; c Epidemiology Branch, National Institute of Environmental Health Sciences, National Institutes of Health, Durham, North Carolina; d Ms Forthun was responsible for the analysis and interpretation of data, and the drafting of the manuscript; Dr Wilcox participated in the analysis and interpretation of data and reviewed and revised the manuscript; Drs Lie and Moster provided advice regarding study design, participated in the interpretation of data, and reviewed and revised the manuscript; Drs Strandberg-Larsen, Nohr, and Surén participated in the interpretation of data and reviewed and revised the manuscript; Dr Tollånes proposed the study, participated in the analysis and interpretation of data, and reviewed and revised the manuscript; and all authors approved the fi nal manuscript as submitted. The prevalence of overweight and obesity among pregnant women is increasing worldwide with adverse effects on maternal and child health. 6 Obese pregnant women (BMI >29.9) have increased risk of gestational diabetes, hypertension, and preeclampsia, and their offspring are at increased risk of preterm birth, macrosomia, complications during delivery, and perinatal death. 6 -9 Maternal obesity is also associated with birth defects, in particular neural tube defects. 10 We used pooled data from 2 large prospective Nordic birth cohorts to investigate the association between BMI before pregnancy and risk of CP in offspring, both overall and for variou...

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“…Intrauterine inflammation leads to a dysregulation of the developing brain, known as fetal inflammatory response syndrome (de Moura, Lisboa, & Passos, 2008), regardless of the gestational age (Burd, Balakrishnan, & Kannan, 2012). The maternal response to lipopolysaccharide (LPS) leads to a fetal inflammatory response mediated by cytokines that has been implicated in the development of a spectrum of neurodevelopmental disorders such as autism and schizophrenia (Meyer, 2011;Meyer et al, 2006).…”

Section: Introductionmentioning

confidence: 99%

Prenatal lipopolysaccharide increases maternal behavior, decreases maternal odor preference, and induces lipopolysaccharide hyporesponsiveness.

Massoco¹,

Kirsten²,

Reis-Silva³

et al. 2013

Psychology & Neuroscience

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The present study investigated whether late maternal inflammation disrupts the mother/pup interaction, resulting in longlasting effects on pup behavior and alterations in biological pathways, thereby programming prepubertal behavior and the pups' inflammatory responses after bacterial endotoxin treatment. Female rats received 100 μg/kg lipopolysaccharide (LPS) or .9% saline solution on gestation day 18. Reproductive performance was observed at birth. On lactation days (LD) 5 and LD 6, respectively, maternal behavior and maternal aggressive behavior were assessed. In pups, maternal odor preference on LD 7, open field behavior on LD 21, and serum tumor necrosis factor α (TNF-α) levels after LPS challenge on LD 21 were investigated. The results showed that prenatal LPS exposure improved maternal care and reduced maternal aggressive behavior but did not alter maternal reproductive performance. Male offspring exhibited increased body weights at birth and reduced maternal odor preference. Lipopolysaccharide challenge increased the duration of immobility in the open field and induced a slight increase in serum TNF-α levels. Prenatal exposure to LPS during late pregnancy improved maternal care, reduced maternal olfactory preference, and induced TNF-α hyporesponsiveness to a single dose of LPS in pups.

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Models of Fetal Brain Injury, Intrauterine Inflammation, and Preterm Birth

Cited by 215 publications

References 69 publications

Impact of prenatal antimicrobial treatment on fetal brain damage due to autogenous fecal peritonitis in Wistar rats: A Histomorphometric Study

Impact of prenatal antimicrobial treatment on fetal brain damage due to autogenous fecal peritonitis in Wistar rats: A Histomorphometric Study

Maternal Prepregnancy BMI and Risk of Cerebral Palsy in Offspring

Prenatal lipopolysaccharide increases maternal behavior, decreases maternal odor preference, and induces lipopolysaccharide hyporesponsiveness.

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