Placenta · 2025
Placental dysfunction and neonatal mortality induced by Salmonella Abortusequi in a murine model of pregestational infection.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Betancourt Diana M, Noto Llana Mariángeles, Garófalo Ailín N, Sarnacki Sebastián H, Cerquetti M Cristina, Bridón Nairobi Hernández, Pustovrh M Carolina, Giacomodonato Mónica N
Аннотация
INTRODUCTION: Salmonella Abortusequi is a host-restricted equine pathogen and a major cause of abortion in mares, threatening reproductive health and industry sustainability. This study was aimed to identify factors that adversely affect placental function, contributing to the development of fetal growth restriction (FGR) and neonatal mortality.
METHODS: CF1 virgin female mice received a pregestational intragastric dose of Salmonella Abortusequi (108 CFU/mouse). On gestational day 18 (GD18), pregnant females were sacrificed, and maternal tissues and fetoplacental units were collected. In a separate group, pregnancy proceeded to term for neonatal outcome assessment.
RESULTS: Salmonella Abortusequi infection impaired placental morphometry and efficiency, leading to FGR and increased neonatal mortality. Offspring from infected dams had persistently low body weight and 40.3 % mortality rate during the first postnatal week. Molecular detection of the invA gene confirmed bacterial presence in fetoplacental units at GD18 and prolonged persistence in maternal spleen and liver up to 90 days post-inoculation. Infection significantly reduced placental claudin-4 gene and protein expression, suggesting a disruption of placental barrier integrity.
DISCUSSION: This study demonstrates that a pregestational infection with Salmonella Abortusequi can exert long-term consequences not only on placental development and fetal growth, but also on neonatal viability and early postnatal development. Importantly, these findings highlight the potential impact of subclinical maternal infections as contributors to reproductive failure and early-life morbidity.
METHODS: CF1 virgin female mice received a pregestational intragastric dose of Salmonella Abortusequi (108 CFU/mouse). On gestational day 18 (GD18), pregnant females were sacrificed, and maternal tissues and fetoplacental units were collected. In a separate group, pregnancy proceeded to term for neonatal outcome assessment.
RESULTS: Salmonella Abortusequi infection impaired placental morphometry and efficiency, leading to FGR and increased neonatal mortality. Offspring from infected dams had persistently low body weight and 40.3 % mortality rate during the first postnatal week. Molecular detection of the invA gene confirmed bacterial presence in fetoplacental units at GD18 and prolonged persistence in maternal spleen and liver up to 90 days post-inoculation. Infection significantly reduced placental claudin-4 gene and protein expression, suggesting a disruption of placental barrier integrity.
DISCUSSION: This study demonstrates that a pregestational infection with Salmonella Abortusequi can exert long-term consequences not only on placental development and fetal growth, but also on neonatal viability and early postnatal development. Importantly, these findings highlight the potential impact of subclinical maternal infections as contributors to reproductive failure and early-life morbidity.