Enteropathogenic Escherichia coli Infection Induces Diarrhea, Intestinal Damage, Metabolic Alterations, and Increased Intestinal Permeability in a Murine Model

Autor: Pedro H. Q. S. Medeiros, Deiziane Viana da Silva Costa, Solanka E. Ledwaba, Natasha Potgieter, David T. Bolick, Jonathan R. Swann, Richard L. Guerrant, Natasa Giallourou, Afsatou Ndama Traore, James P. Nataro
Jazyk: angličtina
Rok vydání: 2020
Předmět:
0301 basic medicine
Chemokine
Antibiotics
lcsh:QR1-502
diarrhea
lcsh:Microbiology
antibiotics
murine model
Pathogenesis
Enteropathogenic Escherichia coli
Mice
Cellular and Infection Microbiology
Diarreia
Escherichia coli Infections
Original Research
biology
Escherichia coli Proteins
enteropathogenic Escherichia coli
Anti-Bacterial Agents
Diarrhea
Infectious Diseases
Antibacterianos
medicine.symptom
Microbiology (medical)
medicine.drug_class
030106 microbiology
Immunology
Virulence
Inflammation
Microbiology
digestive system
Permeability
03 medical and health sciences
medicine
Animals
Escherichia coli Enteropatogênica
Intestinal permeability
biochemical phenomena
metabolism
and nutrition
medicine.disease
bacterial infections and mycoses
Mice
Inbred C57BL
Inflamação
Disease Models
Animal
030104 developmental biology
enteropathy
inflammation
biology.protein
bacteria
Zdroj: Frontiers in Cellular and Infection Microbiology
Frontiers in Cellular and Infection Microbiology, Vol 10 (2020)
Repositório Institucional da Universidade Federal do Ceará (UFC)
Universidade Federal do Ceará (UFC)
instacron:UFC
ISSN: 2235-2988
Popis: Enteropathogenic E. coli (EPEC) are recognized as one of the leading bacterial causes of infantile diarrhea worldwide. Weaned C57BL/6 mice pretreated with antibiotics were challenged orally with wild-type EPEC or escN mutant (lacking type 3 secretion system) to determine colonization, inflammatory responses and clinical outcomes during infection. Antibiotic disruption of intestinal microbiota enabled efficient colonization by wild-type EPEC resulting in growth impairment and diarrhea. Increase in inflammatory biomarkers, chemokines, cellular recruitment and pro-inflammatory cytokines were observed in intestinal tissues. Metabolomic changes were also observed in EPEC infected mice with changes in tricarboxylic acid (TCA) cycle intermediates, increased creatine excretion and shifts in gut microbial metabolite levels. In addition, by 7 days after infection, although weights were recovering, EPEC-infected mice had increased intestinal permeability and decreased colonic claudin-1 levels. The escN mutant colonized the mice with no weight loss or increased inflammatory biomarkers, showing the importance of the T3SS in EPEC virulence in this model. In conclusion, a murine infection model treated with antibiotics has been developed to mimic clinical outcomes seen in children with EPEC infection and to examine potential roles of selected virulence traits. This model can help in further understanding mechanisms involved in the pathogenesis of EPEC infections and potential outcomes and thus assist in the development of potential preventive or therapeutic interventions.
Databáze: OpenAIRE
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