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A mouse model reproducing the pathophysiology of neonatal group B streptococcal infection

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Resumo:Group B streptococcal (GBS) meningitis remains a devastating disease. The absence of an animal model reproducing the natural infectious process has limited our understanding of the disease and, consequently, delayed the development of effective treatments. We describe here a mouse model in which bacteria are transmitted to the offspring from vaginally colonised pregnant females, the natural route of infection. We show that GBS strain BM110, belonging to the CC17 clonal complex, is more virulent in this vertical transmission model than the isogenic mutant BM110∆cylE, which is deprived of hemolysin/cytolysin. Pups exposed to the more virulent strain exhibit higher mortality rates and lung inflammation than those exposed to the attenuated strain. Moreover, pups that survive to BM110 infection present neurological developmental disability, revealed by impaired learning performance and memory in adulthood. The use of this new mouse model, that reproduces key steps of GBS infection in newborns, will promote a better understanding of the physiopathology of GBS-induced meningitis.
Autores principais:Bonifácio Andrade, Elva
Outros Autores:Magalhães, Ana; Puga, Ana; Costa, Madalena; Bravo, Joana; Portugal, Camila Cabral; Ribeiro, Adília; Correia-Neves, Margarida; Faustino, Augusto; Firon, Arnaud; Trieu-Cuot, Patrick; Summavielle, Teresa; Ferreira, Paula
Assunto:Animals Behavior, Animal Body Weight Hemolysin Proteins Inflammation Maze Learning Meningitis Meningitis, Bacterial Mice Mice, Inbred BALB C Perforin Pregnancy Pregnancy, Animal Streptococcal Infections Streptococcus agalactiae Disease Models, Animal Infectious Disease Transmission, Vertical
Ano:2018
País:Portugal
Tipo de documento:artigo
Tipo de acesso:acesso aberto
Instituição associada:Instituto Politécnico do Porto
Idioma:inglês
Origem:Repositório Científico do Instituto Politécnico do Porto
Descrição
Resumo:Group B streptococcal (GBS) meningitis remains a devastating disease. The absence of an animal model reproducing the natural infectious process has limited our understanding of the disease and, consequently, delayed the development of effective treatments. We describe here a mouse model in which bacteria are transmitted to the offspring from vaginally colonised pregnant females, the natural route of infection. We show that GBS strain BM110, belonging to the CC17 clonal complex, is more virulent in this vertical transmission model than the isogenic mutant BM110∆cylE, which is deprived of hemolysin/cytolysin. Pups exposed to the more virulent strain exhibit higher mortality rates and lung inflammation than those exposed to the attenuated strain. Moreover, pups that survive to BM110 infection present neurological developmental disability, revealed by impaired learning performance and memory in adulthood. The use of this new mouse model, that reproduces key steps of GBS infection in newborns, will promote a better understanding of the physiopathology of GBS-induced meningitis.