Publikationsdatenbank

Neural injury and repair in a novel neonatal mouse model of Listeria monocytogenes meningoencephalitis (2021)

Art

Zeitschriftenartikel / wissenschaftlicher Beitrag

Autoren

Seele, Jana

Ballüer, Melissa

Tauber, Simone C.

Bunkowski, Stephanie

Schulz, Katja

Stadelmann, Christine

Beineke, Andreas

Pägelow, Dennis (WE 7)

Fulde, Marcus (WE 7)

Nau, Roland

Quelle

Journal of neuropathology and experimental neurology : official journal of the American Association of Neuropathologists

Bandzählung: 80

Heftzählung: 9

Seiten: 861 – 867

ISSN: 0022-3069

Sprache

Englisch

Verweise

URL (Volltext): https://academic.oup.com/jnen/article/80/9/861/6364775?login=true

DOI: 10.1093/jnen/nlab079

Pubmed: 34486672

Kontakt

Institut für Mikrobiologie und Tierseuchen

Robert-von-Ostertag-Str. 7-13
14163 Berlin
+49 30 838 51843 / 66949
mikrobiologie@vetmed.fu-berlin.de

Abstract / Zusammenfassung

To improve the therapy of neonatal central nervous system infections, well-characterized animal models are urgently needed. The present study analyzes neuropathological alterations with particular focus on neural injury and repair in brains of neonatal mice with Listeria monocytogenes (LM) meningitis/meningoencephalitis using a novel nasal infection model. The hippocampal formation and frontal cortex of 14 neonatal mice with LM meningitis/meningoencephalitis and 14 uninfected controls were analyzed by histology, immunohistochemistry, and in situ tailing for morphological alterations. In the dentate gyrus of the hippocampal formation of mice with LM meningitis/meningoencephalitis, an increased density of apoptotic neurons visualized by in situ tailing (p = 0.04) and in situ tailing plus immunohistochemistry for activated Caspase-3 (p < 0.0001) was found. A decreased density of dividing cells stained with an anti-PCNA-antibody (p < 0.0001) and less neurogenesis visualized by anti-calretinin (p < 0.0001) and anti-calbindin (p = 0.01) antibodies were detected compared to uninfected controls. The density of microglia was higher in LM meningitis (p < 0.0001), while the density of astrocytes remained unchanged. Infiltrating monocytes and neutrophilic granulocytes likely contributed to tissue damage. In conclusion, in the brains of LM-infected mice a strong immune response was observed which led to neuronal apoptosis and an impaired neural regeneration. This model appears very suitable to study therapies against long-term sequelae of neonatal LM meningitis.