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    Major advances in understanding the pathophysiology of neonatal group B streptococcal infections

    Team directed by Claire Poyart and Agnès Fouet

    The study carried out under the direction of Asmaa Tazi within the "Bacteria and Perinatality" team

    within the “département hospitalo-universitaire Risks and Pregnancy" (Cochin AP-HP hospital and Institut Cochin), shows that the hypervirulence of Group B streptococci (Streptococcus agalactiae or "GBS") is potentiated by the high hormonal levels observed in newborns over 7 days of age, which can result in the most serious form of infection in the newborn, meningitis. This work has been published on November 2019 in the eLIFE journal.


    Group B Streptococcus (Streptococcus agalactiae or "GBS") is the leading cause of invasive bacterial neonatal infection. A viral clone specific to the newborn, clone CC17, is responsible for almost 80% of cases of meningitis and of almost all late infections that occur beyond one week of life, mostly between three weeks and two months. The invasion pathway and the factors involved in the pathophysiology of GBS CC17 infection are still poorly understood.

    In this work published in eLIFE, the impact of maternal hormones estradiol (E2) and progesterone (P4), that permeate the fetus throughout pregnancy and the first months of newborn life, has been studied. Using multiple experimental approaches to reproduce human neonatal infection, researchers have shown in a murine model that elevated levels of estradiol (E2) and progesterone (P4) found beyond 7 days of birth specifically favored severity of GBS CC17 meningitis after oral infection.


    This work demonstrates that GBS CC17 crosses the intestinal barrier via M cells (specialized epithelial cells allowing passage of bacteria or antigens) in a process dependent on the Srr2 surface protein specific for the CC17 hypervirulent clone.

    Finally, this study shows that the concentrations of estradiol (E2) and progesterone (P4) found in the newborn beyond 7 days of life promote the differentiation of M cells and the crossing of the intestinal barrier by this streptococcus, which brings for the first time an explanation to the very particular susceptibility of newborns to this bacterium.


    These results represent a breakthrough in understanding the pathophysiology of late-onset GBS infections and pave the way for future research into the pathophysiology of neonatal infections caused by other pathogens.



    Perinatal hormones favor CC17 group B Streptococcus intestinal translocation through M cells and hypervirulence in neonates. Hays C, Touak G, Bouaboud A, Fouet A, Guignot J, Poyart C, Tazi A*. eLIFE. 2019 Nov 11;8. pii: e48772.  doi: 10.7554/eLife.48772.


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