Disruption of blood-brain barrier by an Escherichia coli isolated from canine septicemia and meningoencephalitis

•E. coli isolate named CEC-GZL17 caused canine septicemia and meningoencephalitis.•A large number of CEC-GZL17 bacteria were observed in the brain tissue.•CEC-GZL17 had the capability of disrupting the blood-brain barrier. Escherichia coli (E. coli) is one of the common pathogenic bacteria in veteri...

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Veröffentlicht in:Comparative immunology, microbiology and infectious diseases microbiology and infectious diseases, 2019-04, Vol.63, p.44-50
Hauptverfasser: Li, Xin, Zhang, Zecai, Chang, Xiaoran, Wang, Xu, Hu, Junying, Lin, Qian, Jia, Yingqi, Yang, Xu, Wang, Xinping
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Sprache:eng
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Zusammenfassung:•E. coli isolate named CEC-GZL17 caused canine septicemia and meningoencephalitis.•A large number of CEC-GZL17 bacteria were observed in the brain tissue.•CEC-GZL17 had the capability of disrupting the blood-brain barrier. Escherichia coli (E. coli) is one of the common pathogenic bacteria in veterinary clinical infection. As an opportunistic microorganism, E. coli normally does not cause diseases. However, it causes infections under certain circumstance to domesticated animal and poultry, resulting in severe diarrhea, septicemia, and respiratory infections. Although there are increasing reports regarding the infections of E. coli to domestic animals and poultry, the infection of E. coli in dogs is relatively less reported, especially on septicemia and meningoencephalitis. Here, we reported the isolation and identification of an E. coli isolate named CEC-GZL17 from dogs characterized by septicemia and sudden death, and found that CEC-GZL17 is able to cause meningoencephalitis. Exploration on the potential mechanism underlying meningoencephalitis demonstrated that CEC-GZL17 infection significantly increases TNF-α expression and inhibits ZO-1 and occludin expressions in brain tissue, indicating that the E coli likely use the mechanism to penetrate the blood-brain barrier via disrupting tight junction architecture, thus leading to the invasion to brain tissue.
ISSN:0147-9571
1878-1667
DOI:10.1016/j.cimid.2019.01.002