scholarly journals In vitro and in vivo effects of hydrolysates from conglycinin on intestinal microbial community of mice after Escherichia coli infection

2007 ◽  
Vol 102 (1) ◽  
pp. 283-289 ◽  
Author(s):  
C.-L. Shen ◽  
W.-H. Chen ◽  
S.-X. Zou
2019 ◽  
Vol 30 (8) ◽  
pp. 1385-1397 ◽  
Author(s):  
Tad Eichler ◽  
Kristin Bender ◽  
Matthew J. Murtha ◽  
Laura Schwartz ◽  
Jackie Metheny ◽  
...  

BackgroundEvidence suggests that antimicrobial peptides, components of the innate immune response, protect the kidneys and bladder from bacterial challenge. We previously identified ribonuclease 7 (RNase 7) as a human antimicrobial peptide that has bactericidal activity against uropathogenic Escherichia coli (UPEC). Functional studies assessing RNase 7’s contributions to urinary tract defense are limited.MethodsTo investigate RNase 7’s role in preventing urinary tract infection (UTI), we quantified urinary RNase 7 concentrations in 29 girls and adolescents with a UTI history and 29 healthy female human controls. To assess RNase 7’s antimicrobial activity in vitro in human urothelial cells, we used siRNA to silence urothelial RNase 7 production and retroviral constructs to stably overexpress RNase 7; we then evaluated UPEC’s ability to bind and invade these cells. For RNase 7 in vivo studies, we developed humanized RNase 7 transgenic mice, subjected them to experimental UTI, and enumerated UPEC burden in the urine, bladder, and kidneys.ResultsCompared with controls, study participants with a UTI history had 1.5-fold lower urinary RNase 7 concentrations. When RNase 7 was silenced in vitro, the percentage of UPEC binding or invading human urothelial cells increased; when cells overexpressed RNase 7, UPEC attachment and invasion decreased. In the transgenic mice, we detected RNase 7 expression in the kidney’s intercalated cells and bladder urothelium. RNase 7 humanized mice exhibited marked protection from UPEC.ConclusionsThese findings provide evidence that RNase 7 has a role in kidney and bladder host defense against UPEC and establish a foundation for investigating RNase 7 as a UTI prognostic marker or nonantibiotic-based therapy.


2008 ◽  
Vol 100 (03) ◽  
pp. 530-541 ◽  
Author(s):  
Leo R. Fitzpatrick ◽  
Jeffrey Small ◽  
Robert A. Hoerr ◽  
Eileen F. Bostwick ◽  
Lynn Maines ◽  
...  

2007 ◽  
Vol 14 (5) ◽  
pp. 585-592 ◽  
Author(s):  
Mélanie Gallois ◽  
Thierry Gidenne ◽  
Christian Tasca ◽  
Cécile Caubet ◽  
Cécile Coudert ◽  
...  

ABSTRACT Enteropathogenic Escherichia coli (EPEC) colibacillosis represents a major cause of lethal diarrhea in young children in developing countries. EPEC strains also infect numerous mammal species and represent a major economical problem in rabbit industry. Protection against this pathogen is a challenging goal both in humans and in other mammal species. Despite a good knowledge of the pathogenicity mechanisms of EPEC, the intrinsic and environmental factors that control the expression of EPEC virulence in mammals remain unknown. For instance, the exacerbated sensitivity of young mammals to EPEC infection is still unexplained. Our goal was to investigate if age or other factors, like milk consumption, could be determinants that trigger the disease. We used rabbits as an animal model to study the role of milk in the sensitivity to an EPEC infection. Weaned and suckling rabbits were orally inoculated with EPEC strain E22 (O103:H2:K−) at 28 days of age, and the evolution of the disease was investigated in the two groups. In addition, in order to better characterize the interactions between milk and EPEC, we determined in vitro bacterial growth and the abilities of EPEC cells to adhere to epithelial cells in the presence of milk. Our results demonstrate a protective role of milk in vivo in association with in vitro antibacterial activity. These effects are independent of the presence of specific anti-EPEC antibodies.


2007 ◽  
Vol 75 (12) ◽  
pp. 5974-5984 ◽  
Author(s):  
John K. Crane ◽  
Tonniele M. Naeher ◽  
Irina Shulgina ◽  
Chengru Zhu ◽  
Edgar C. Boedeker

ABSTRACT Enteropathogenic Escherichia coli (EPEC) infection triggers the release of ATP from host intestinal cells, and the ATP is broken down to ADP, AMP, and adenosine in the lumen of the intestine. Ecto-5′-nucleotidase (CD73) is the main enzyme responsible for the conversion of 5′-AMP to adenosine, which triggers fluid secretion from host intestinal cells and also has growth-promoting effects on EPEC bacteria. In a recent study, we examined the role of the host enzyme CD73 in EPEC infection by testing the effect of ecto-5′-nucleotidase inhibitors. Zinc was a less potent inhibitor of ecto-5′-nucleotidase in vitro than the nucleotide analog α,β-methylene-ADP, but in vivo, zinc was much more efficacious in preventing EPEC-induced fluid secretion in rabbit ileal loops than α,β-methylene-ADP. This discrepancy between the in vitro and in vivo potencies of the two inhibitors prompted us to search for potential targets of zinc other than ecto-5′-nucleotidase. Zinc, at concentrations that produced little or no inhibition of EPEC growth, caused a decrease in the expression of EPEC protein virulence factors, such as bundle-forming pilus (BFP), EPEC secreted protein A, and other EPEC secreted proteins, and reduced EPEC adherence to cells in tissue culture. The effects of zinc were not mimicked by other transition metals, such as manganese, iron, copper, or nickel, and the effects were not reversed by an excess of iron. Quantitative real-time PCR showed that zinc reduced the abundance of the RNAs encoded by the bfp gene, by the plasmid-encoded regulator (per) gene, by the locus for the enterocyte effacement (LEE)-encoded regulator (ler) gene, and by several of the esp genes. In vivo, zinc reduced EPEC-induced fluid secretion into ligated rabbit ileal loops, decreased the adherence of EPEC to rabbit ileum, and reduced histopathological damage such as villus blunting. Some of the beneficial effects of zinc on EPEC infection appear to be due to the action of the metal on EPEC bacteria as well as on the host.


2022 ◽  
Vol 53 (1) ◽  
pp. 139-145
Author(s):  
fateme Andalib ◽  
Hojjat Baghshahi ◽  
Mohammadreza Memarzadeh ◽  
Hossein Akbari

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