Affiliation:
1. Institute of Hygiene and Microbiology, University of Wuerzburg, Wuerzburg, Germany
Abstract
ABSTRACT
Microbial pathogens have developed several mechanisms to modulate and interfere with host cell cycle progression. In this study, we analyzed the effect of the human pathogen
Neisseria meningitidis
on the cell cycle of epithelial cells. Two pathogenic isolates, as well as two carrier isolates, were tested for their ability to adhere to and invade into the epithelial cell lines Detroit 562 and NP69 and to modulate the cell cycle. We found that all isolates adhered equally well to both Detroit 562 and NP69 cells, whereas the carrier isolates were significantly less invasive. Using propidium iodide staining and 5-ethynyl-2′-deoxyuridine pulse-labeling, we provide evidence that meningococcal infection arrested cells in the G
1
phase of the cell cycle at 24 h postinfection. In parallel, a significant decrease of cells in the S phase was observed. Interestingly, G
1
-phase arrest was only induced after infection with live bacteria but not with heat-killed bacteria. By Western blotting we demonstrate that bacterial infection resulted in a decreased protein level of the cell cycle regulator cyclin D1, whereas cyclin E expression levels were increased. Furthermore,
N. meningitidis
infection induced an accumulation of the cyclin-dependent kinase inhibitor (CKI) p21
WAF1/CIP1
that was accompanied by a redistribution of this CKI to the cell nucleus, as shown by immunofluorescence analysis. Moreover, the p27
CIP1
CKI was redistributed and showed punctate foci in infected cells. In summary, we present data that
N. meningitidis
can interfere with the processes of host cell cycle regulation.
Funder
Deutsche Forschungsgemeinschaft
Publisher
American Society for Microbiology
Subject
Infectious Diseases,Immunology,Microbiology,Parasitology
Cited by
10 articles.
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