Hyperactive behavior in female rats <i>in utero</i>‐exposed to group B <i>Streptococcus</i>‐induced inflammation

Allard, Marie-Julie; Brochu, Marie-Elsa; Bergeron, Julie; Sébire, Guillaume

doi:10.1016/j.ijdevneu.2018.06.005

Cited by 12 publications

(15 citation statements)

References 56 publications

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“…A recent study also indicates that prenatal TLR7 activation results in sex-dependent neurobehavioral abnormalities and specific sex-dependent gene regulation in the dorsal striatum [180]. In addition to studies using specific TLR ligands, Group B Streptococcus (GBS) induced maternal infection during pregnancy in rats has been linked to increased spontaneous locomotor activity and decreased inhibition, particularly in female offspring [181].…”

Section: Animal Models Of Perinatal Inflammation: Behavioral Abnormentioning

confidence: 99%

Sex-Dependent Effects of Perinatal Inflammation on the Brain: Implication for Neuro-Psychiatric Disorders

Ardalan

Chumak

Vexler

et al. 2019

IJMS

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Individuals born preterm have higher rates of neurodevelopmental disorders such as schizophrenia, autistic spectrum, and attention deficit/hyperactivity disorders. These conditions are often sexually dimorphic and with different developmental trajectories. The etiology is likely multifactorial, however, infections both during pregnancy and in childhood have emerged as important risk factors. The association between sex- and age-dependent vulnerability to neuropsychiatric disorders has been suggested to relate to immune activation in the brain, including complex interactions between sex hormones, brain transcriptome, activation of glia cells, and cytokine production. Here, we will review sex-dependent effects on brain development, including glia cells, both under normal physiological conditions and following perinatal inflammation. Emphasis will be given to sex-dependent effects on brain regions which play a role in neuropsychiatric disorders and inflammatory reactions that may underlie early-life programming of neurobehavioral disturbances later in life.

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Section: Animal Models Of Perinatal Inflammation: Behavioral Abnormentioning

confidence: 99%

Sex-Dependent Effects of Perinatal Inflammation on the Brain: Implication for Neuro-Psychiatric Disorders

Ardalan

Chumak

Vexler

et al. 2019

IJMS

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“…Our lab has developed rat models of GBS-induced chorioamnionitis. We previously showed that male rat offspring presented autistic-like traits, in sharp contrast with hyperactive behaviour in females 32–34 . The GBS-exposed offspring presented dysmyelinated forebrain white matter reminiscent of those observed in human perinatal injuries 32–34 .…”

Section: Introductionmentioning

confidence: 96%

“…We previously showed that male rat offspring presented autistic-like traits, in sharp contrast with hyperactive behaviour in females 32–34 . The GBS-exposed offspring presented dysmyelinated forebrain white matter reminiscent of those observed in human perinatal injuries 32–34 . In this same model, end-gestational GBS-induced acute chorioamnionitis was characterised by a more prominent PMN infiltration in placentas of males compared to female offspring, raising the hypothesis of a relationship between the sex-biased inflammatory response and the distinct neurobehavioural phenotypes 32 .…”

Section: Introductionmentioning

confidence: 96%

Sex-specific maternofetal innate immune responses triggered by group B Streptococci

Allard

Giraud

Segura

et al. 2019

Sci Rep

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Group B Streptococcus (GBS) is one of the most common bacteria isolated in human chorioamnionitis, which is a major risk factor for premature birth and brain injuries. Males are at greater risk than females for developing lifelong neurobehavioural disorders, although the origins of this sex bias remain poorly understood. We previously showed that end-gestational inflammation triggered by GBS led to early neurodevelopmental impairments mainly in the male rat progeny. Identifying key inflammatory players involved in maternofetal immune activation by specific pathogens is critical to develop appropriate novel therapeutic interventions. We aimed to map out the GBS-induced profile of innate immune biomarkers in the maternal-placental-fetal axis, and to compare this immune profile between male and female tissues. We describe here that the GBS-induced immune signalling involved significantly higher levels of interleukin (IL)-1β, cytokine-induced neutrophil chemoattractant-1 (CINC-1/CXCL1) and polymorphonuclear cells (PMNs) infiltration in male compared to female maternofetal tissues. Although male – but not female – fetuses presented increased levels of IL-1β, fetuses from both sexes in-utero exposed to GBS had increased levels of TNF-α in their circulation. Levels of IL-1β detected in fetal sera correlated positively with the levels found in maternal circulation. Here, we report for the first time that the maternofetal innate immune signalling induced by GBS presents a sexually dichotomous profile, with more prominent inflammation in males than females. These sex-specific placental and fetal pro-inflammatory responses are in keeping with the higher susceptibility of the male population for preterm birth, brain injuries and neurodevelopmental disorders such as cerebral palsy and autism spectrum disorders.

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“…Allard et al . showed that female rats exposed to in utero placental inflammation showed hyperactive behavior after puberty 52 . IPA analysis of our data indicates that HCA differentially expressed genes in the IL-17 signaling pathway, IL-17A signaling in airway cells, and IL-17A signaling in fibroblasts.…”

Section: Discussionmentioning

confidence: 99%

Histological Chorioamnionitis Induces Differential Gene Expression in Human Cord Blood Mononuclear Leukocytes from Term Neonates

Betal

Murthy

Favara

et al. 2019

Sci Rep

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Histological chorioamnionitis (HCA) is an infection of fetal membranes and complicates 5.2% to 28.5% of all live births. HCA is associated with increased mortality and morbidity in both premature and term neonates. Exposure to HCA may have long-term consequences, including an increased risk for allergic disorders and asthma later in childhood, the mechanism(s) of which are still not yet well understood. The objective of this study was to determine the mRNA transcriptome of cord blood mononuclear leukocytes from term neonates to identify key genes and pathways involved in HCA. We found 366 differentially expressed probe IDs with exposure to HCA (198 upregulated, 168 downregulated). These transcriptomes included novel genes and pathways associated with exposure to HCA. The differential gene expression included key genes regulating inflammatory, immune, respiratory and neurological pathways, which may contribute to disorders in those pathways in neonates exposed to HCA. Our data may lead to understanding of the role of key genes and pathways identified on the long-term sequelae related to exposure to HCA, as well as to identifying potential markers and therapies to prevent HCA-associated complications.

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Hyperactive behavior in female rats in utero‐exposed to group B Streptococcus‐induced inflammation

Cited by 12 publications

References 56 publications

Sex-Dependent Effects of Perinatal Inflammation on the Brain: Implication for Neuro-Psychiatric Disorders

Sex-Dependent Effects of Perinatal Inflammation on the Brain: Implication for Neuro-Psychiatric Disorders

Sex-specific maternofetal innate immune responses triggered by group B Streptococci

Histological Chorioamnionitis Induces Differential Gene Expression in Human Cord Blood Mononuclear Leukocytes from Term Neonates

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