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Meningeal γδ T cells facilitate bacterial entry into the brain in neonatal meningitis and trigger long-term behavioural sequelae

2025-11-09Preprint Acesso aberto
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dc.contributor.authorLorga, Inês
dc.contributor.authorSoares, Joana
dc.contributor.authorBravo, Joana
dc.contributor.authorMesquita, Pedro
dc.contributor.authorRibeiro, Nuno
dc.contributor.authorRodrigues, João
dc.contributor.authorHassan, Ahmed
dc.contributor.authorMesquita, Morgana
dc.contributor.authorCavadas, Bruno
dc.contributor.authorGeorgiev, Hristo
dc.contributor.authorMagalhães, Ana
dc.contributor.authorSummavielle, Teresa
dc.contributor.authorVilanova, Manuel
dc.contributor.authorRibot, Julie C.
dc.contributor.authorAndrade, Elva Bonifácio
dc.contributor.authorBonifácio Andrade, Elva
dc.contributor.authorSummavielle, Teresa
dc.date.accessioned2026-06-29T09:26:39Z
dc.date.available2026-06-29T09:26:39Z
dc.date.issued2025-11-09
dc.description.abstractNeonatal bacterial meningitis is a life-threatening condition and a leading cause of neurodevelopmental impairment among survivors. Despite its prevalence, the role of meningeal immunity on disease pathology during early life remains largely unexplored. Using a clinically relevant mouse model of neonatal group B streptococcal meningitis and single-cell RNA sequencing, we observed that IL-17A (IL-17)-producing γδ T cells (γδ17 T cells) accumulate in the meninges during the acute phase of infection and persist throughout the lifespan. Importantly, mice deficient in γδ T cells or in IL-17 show a significantly lower bacterial colonisation in the brain parenchyma, and IL-17 neutralisation in the cerebrospinal fluid leads to a similar phenotype. Reduced blood-brain barrier permeability in the absence of γδ T cells results in decreased bacterial invasion and diminished microglia activation. Wild-type but not γδ T cell-deficient mice surviving infection exhibit increased hyperactivity and open space anxiety during early adulthood, a behavioural profile that may reflect attention deficit and hyperactivity (ADHD)-like tendencies. Altogether, these findings establish a pathogenic role for meningeal γδ17 T cells in early life, uncovering a key mechanism that drives long-term sequelae in GBS neonatal meningitis.eng
dc.identifier.citationLorga, I., Soares, J., Bravo, J., Mesquita, P., Ribeiro, N., Rodrigues, J., Hassan, A., Mesquita, M., Cavadas, B., Georgiev, H., Magalhães, A., Summavielle, T., Vilanova, M., Ribot, J. C., & Andrade, E. B. (2025). Meningeal γδ T cells facilitate bacterial entry into the brain in neonatal meningitis and trigger long-term behavioural sequelae (p. 2025.11.07.686929). bioRxiv. https://doi.org/10.1101/2025.11.07.686929
dc.identifier.doi10.1101/2025.11.07.686929
dc.identifier.eissn2692-8205
dc.identifier.urihttp://hdl.handle.net/10400.22/32525
dc.language.isoeng
dc.peerreviewedno
dc.relation.hasversionhttps://www.biorxiv.org/content/10.1101/2025.11.07.686929v1
dc.rights.uriN/A
dc.subjectGroup B Streptococcus
dc.subjectMeninges
dc.subjectNeonatal meningitis
dc.subjectγδ T cells
dc.subjectIL-17
dc.subjectADHD
dc.titleMeningeal γδ T cells facilitate bacterial entry into the brain in neonatal meningitis and trigger long-term behavioural sequelaeeng
dc.typepreprint
dspace.entity.typePublication
oaire.citation.titlebioRxiv
oaire.versionhttp://purl.org/coar/version/c_71e4c1898caa6e32
person.familyNameBonifácio Andrade
person.familyNameSummavielle
person.givenNameElva
person.givenNameTeresa
person.identifier677706
person.identifier.ciencia-id511C-11AA-7980
person.identifier.ciencia-idC41E-0816-5C85
person.identifier.orcid0000-0002-1941-580X
person.identifier.orcid0000-0003-2548-6281
person.identifier.ridC-9776-2012
person.identifier.scopus-author-id6603092949
relation.isAuthorOfPublicatione3b8883f-57b2-4b83-afa1-88e663ed8d1f
relation.isAuthorOfPublication207ee2de-85a0-4144-9e7e-b376c600e065
relation.isAuthorOfPublication.latestForDiscoverye3b8883f-57b2-4b83-afa1-88e663ed8d1f

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