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Updated: Jun 23, 2026
Visualisation and Quantification of Intracellular Interactions of Neisseria meningitidis and Human α-actinin by Confocal Imaging
Published on: October 24, 2010
OmpA is the critical component for Escherichia coli invasion-induced astrocyte activation
Hsueh-Hsia Wu1, Yi-Yuan Yang, Wen-Shyang Hsieh
1Graduate Institute and Department of Microbiology, College of Medicine, National Taiwan University, Taipei, Taiwan.
Abstract:
Escherichia coli is the major Gram-negative bacterial pathogen in neonatal meningitis. Outer membrane protein A (OmpA) is a conserved major protein in the E. coli outer membrane and is involved in several host-cell interactions. To characterize the role of OmpA in the invasion of astrocytes by E. coli, we investigated OmpA-positive and OmpA-negative E. coli strains. Outer membrane protein A E44, E105, and E109 strains adhered to and invaded C6 glioma cells 10- to 15-fold more efficiently than OmpA-negative strains. Actin rearrangement, protein tyrosine kinase, and phosphoinositide 3-kinase activation were required for OmpA-mediated invasion by E. coli. In vitro infection of C6 cells and intracerebral injection into mice of the E44 strain induced expression of the astrocyte differentiation marker glial fibrillary acidic protein and the inflammatory mediators cyclooxygenase 2 and nitric oxide synthase 2. After intracerebral infection with E44, all C57BL/6 mice died within 36hours, whereas 80% of mice injected with E44 premixed with recombinant OmpA protein survived. Astrocyte activation and neutrophil infiltration were reduced in brain tissue sections in the mice given OmpA. Taken together, these data suggest that OmpA-mediated invasion plays an important role in the early stage of E.coli-induced brain damage, and that it may have therapeutic use in E. coli meningitis.
Insights
Outer membrane protein A (OmpA) facilitates Escherichia coli invasion of brain cells, contributing to meningitis. Therapeutic use of OmpA may reduce E. coli-induced brain damage and improve survival rates in neonatal meningitis.
Area of Science:
- Neuroscience
- Microbiology
- Immunology
Background:
- Escherichia coli is a primary cause of Gram-negative bacterial neonatal meningitis.
- Outer membrane protein A (OmpA) is a key E. coli outer membrane protein involved in host-cell interactions.
Purpose of the Study:
- To investigate the role of OmpA in E. coli invasion of astrocytes.
- To evaluate the therapeutic potential of OmpA in E. coli meningitis.
Main Methods:
- Compared OmpA-positive and OmpA-negative E. coli strains for adherence and invasion of C6 glioma cells.
- Assessed the involvement of actin rearrangement, protein tyrosine kinase, and phosphoinositide 3-kinase in OmpA-mediated invasion.
- Infected C6 cells and mice intracerebrally with E. coli E44 strain, analyzing astrocyte and inflammatory marker expression.
- Evaluated the survival rates and brain tissue pathology in mice treated with OmpA.
Main Results:
- OmpA-positive E. coli strains showed 10- to 15-fold greater adherence and invasion of C6 cells compared to OmpA-negative strains.
- OmpA-mediated invasion requires actin rearrangement, protein tyrosine kinase, and phosphoinositide 3-kinase activation.
- E. coli E44 infection induced glial fibrillary acidic protein, cyclooxygenase 2, and nitric oxide synthase 2 expression.
- Intracerebral E44 infection led to high mortality in mice, while OmpA administration improved survival and reduced brain inflammation.
Conclusions:
- OmpA-mediated invasion is crucial in the early stages of E. coli-induced brain damage.
- OmpA demonstrates therapeutic potential for treating E. coli meningitis by mitigating brain injury and enhancing survival.
