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Transcellular traversal of the blood‐brain barrier by the pathogenic Propionibacterium acnes
Author(s) -
Lu Xuetao,
Qi Xianlong,
Yi Xiuli,
Jian Zhe,
Gao Tianwen
Publication year - 2019
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.28132
Subject(s) - transcellular , propionibacterium acnes , blood–brain barrier , in vitro , microbiology and biotechnology , paracellular transport , biology , chemistry , bacteria , permeability (electromagnetism) , biochemistry , membrane , genetics , neuroscience , central nervous system
Background Propionibacterium acnes ( P. acnes ) is an anaerobe commonly stay in the body as part of the commensal microbiota, and a dominant bacterium of the human skin and hair follicles. It has been found that this bacterium could participate in brain inflammation that causes Alzheimer's disease (AD) and Parkinson's disease (PD). But how P. acnes invade the brain remains elusive. Methods We established the in vitro blood‐brain barrier (BBB) model by culturing the HBMEC/D3 cell line on collagen‐coated PFTE membrane. The BBB model was verified by the transepithelial electrical resistance (TEER) and horseradish peroxidase (HRP) permeability rate, and observed by the scanning electron microscope (SEM), transmission electron microscope (TEM), as well as confocal microscope. The P. acnes was then cocultured with the in vitro BBB model and the permeability of P. acnes was measured by counting the bacteria clones collected from the lower chamber of the model. Results High local concentration of P. acnes invaded the in vitro BBB model through the transcellular traversal pathway. The permeability for P. acnes was increased by the treatment of lipopolysaccharide (LPS), but not mannitol. P. acnes invasion elevated the expression of cell adhesion molecules E‐selectin, ICAM‐1, and VCAM‐1 in HBMEC cells. Conclusion P. acnes has the ability to penetrate the brain though transcellular invasion of the blood‐brain barrier.