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Causal role of group B Streptococcus-induced acute chorioamnionitis in intrauterine growth retardation and cerebral palsy-like impairments

Published online by Cambridge University Press:  10 January 2019

M.-J. Allard
Affiliation:
Department of Pediatrics, McGill University, Montreal, QC, Canada
M.-E. Brochu
Affiliation:
Department of Pediatrics, Université de Sherbrooke, Sherbrooke, QC, Canada
J. D. Bergeron
Affiliation:
Department of Pediatrics, Université de Sherbrooke, Sherbrooke, QC, Canada
M. Segura
Affiliation:
Department of Infectiology and Microbiology, Université de Montréal, Saint-Hyacinthe, QC, Canada
G. Sébire*
Affiliation:
Department of Pediatrics, McGill University, Montreal, QC, Canada Department of Pediatrics, Université de Sherbrooke, Sherbrooke, QC, Canada
*
Address for correspondence: Dr G. Sébire, Research Institute of the McGill University Health Centre – Glen site, 1001, Decarie Boulevard, Montreal, QC, Canada H4A 3J1. E-mail: [email protected]

Abstract

Chorioamnionitis and intrauterine growth retardation (IUGR) are risk factors for cerebral palsy (CP). Common bacteria isolated in chorioamnionitis include group B Streptococcus (GBS) serotypes Ia and III. Little is known about the impact of placental inflammation induced by different bacteria, including different GBS strains. We aimed to test the impact of chorioamnionitis induced by two common GBS serotypes (GBSIa and GBSIII) on growth and neuromotor outcomes in the progeny. Dams were exposed at the end of gestation to either saline, inactivated GBSIa or GBSIII. Inactivated GBS bacteria invaded placentas and triggered a chorioamnionitis featured by massive polymorphonuclear cell infiltrations. Offspring exposed to GBSIII – but not to GBSIa – developed IUGR, persisting beyond adolescent age. Male rats in utero exposed to GBSIII traveled a lower distance in the Open Field test, which was correlating with their level of IUGR. GBSIII-exposed rats presented decreased startle responses to acoustic stimuli beyond adolescent age. GBS-exposed rats displayed a dysmyelinated white matter in the corpus callosum adjacent to thinner primary motor cortices. A decreased density of microglial cells was detected in the mature corpus callosum of GBSIII-exposed males – but not females – which was correlating positively with the primary motor cortex thickness. Altogether, our results demonstrate a causal link between pathogen-induced acute chorioamnionitis and (1) IUGR, (2) serotype- and sex-specific neuromotor impairments and (3) abnormal development of primary motor cortices, dysmyelinated white matter and decreased density of microglial cells.

Type
Brief Report
Copyright
© Cambridge University Press and the International Society for Developmental Origins of Health and Disease 2019 

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