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

Comp Immunol Microbiol Infect Dis. 2019 Apr:63:44-50. doi: 10.1016/j.cimid.2019.01.002. Epub 2019 Jan 9.

Abstract

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.

Keywords: Blood-brain barrier; Dogs; Escherichia coli; Meningoencephalitis; Septicemia.

MeSH terms

  • Animals
  • Blood-Brain Barrier / microbiology*
  • Blood-Brain Barrier / pathology
  • Brain / metabolism
  • Dog Diseases / microbiology
  • Dogs
  • Escherichia coli / pathogenicity*
  • Escherichia coli Infections / pathology
  • Escherichia coli Infections / veterinary*
  • Meningoencephalitis / microbiology
  • Meningoencephalitis / pathology*
  • Meningoencephalitis / veterinary
  • Mice
  • Occludin / biosynthesis
  • Sepsis / microbiology
  • Sepsis / pathology*
  • Sepsis / veterinary
  • Tight Junctions / microbiology*
  • Tight Junctions / pathology
  • Tumor Necrosis Factor-alpha / biosynthesis
  • Zonula Occludens-1 Protein / biosynthesis

Substances

  • OCLN protein, human
  • Occludin
  • TJP1 protein, human
  • TNF protein, human
  • Tumor Necrosis Factor-alpha
  • Zonula Occludens-1 Protein