The phosphoproteome of choroid plexus epithelial cells following infection with Neisseria meningitidis

Rosanna Herold; Lea Denzer; Walter Muranyi; Carolin Stump-Guthier; Hiroshi Ishikawa; Horst Schroten; Christian Schwerk

doi:10.3389/fcimb.2023.1113528

The phosphoproteome of choroid plexus epithelial cells following infection with Neisseria meningitidis

Front Cell Infect Microbiol. 2023 Mar 31:13:1113528. doi: 10.3389/fcimb.2023.1113528. eCollection 2023.

Authors

Rosanna Herold^{1

2}, Lea Denzer^{1

2}, Walter Muranyi^{1

2}, Carolin Stump-Guthier^{1

2}, Hiroshi Ishikawa³, Horst Schroten^{1

2}, Christian Schwerk^{1

2}

Affiliations

¹ Pediatric Infectious Diseases, Department of Pediatrics, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.
² European Center for Angioscience, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.
³ Laboratory of Clinical Regenerative Medicine, Department of Neurosurgery, Faculty of Medicine, University of Tsukuba, Tsukuba, Japan.

Abstract

The Gram-negative bacterium Neisseria meningitidis, which causes meningitis in humans, has been demonstrated to manipulate or alter host signalling pathways during infection of the central nervous system (CNS). However, these complex signalling networks are not completely understood. We investigate the phosphoproteome of an in vitro model of the blood-cerebrospinal fluid barrier (BCSFB) based on human epithelial choroid plexus (CP) papilloma (HIBCPP) cells during infection with the N. meningitidis serogroup B strain MC58 in presence and absence of the bacterial capsule. Interestingly, our data demonstrates a stronger impact on the phosphoproteome of the cells by the capsule-deficient mutant of MC58. Using enrichment analyses, potential pathways, molecular processes, biological processes, cellular components and kinases were determined to be regulated as a consequence of N. meningitidis infection of the BCSFB. Our data highlight a variety of protein regulations that are altered during infection of CP epithelial cells with N. meningitidis, with the regulation of several pathways and molecular events only being detected after infection with the capsule-deficient mutant. Mass spectrometry proteomics data are available via ProteomeXchange with identifier PXD038560.

Keywords: Neisseria meningitidis; blood-cerebrospinal fluid barrier; host innate signaling; host pathogen interaction; meningitis; phosphoproteome.

Publication types

Research Support, Non-U.S. Gov't

MeSH terms

Blood-Brain Barrier / microbiology
Cell Line, Tumor
Choroid Plexus / microbiology
Epithelial Cells / microbiology
Humans
Neisseria meningitidis* / physiology

Grants and funding

For the publication fee we acknowledge financial support by Deutsche Forschungsgemeinschaft within the funding programme “Open Access Publikationskosten” as well as by Heidelberg University.