Apple Flavonoid Phloretin Inhibits Escherichia coli O157:H7 Biofilm Formation and Ameliorates Colon Inflammation in Rats

Title
Apple Flavonoid Phloretin Inhibits Escherichia coli O157:H7 Biofilm Formation and Ameliorates Colon Inflammation in Rats
Author(s)
이진태김정애조무환윤형돈이진형이창수[이창수]수실레그미[수실레그미]
Keywords
HEMOLYTIC-UREMIC SYNDROME; GENE-EXPRESSION; BOWEL-DISEASE; O157-H7; ACID; PATHOGENESIS; ANTIOXIDANT; RESISTANCE; COMMENSAL; ADHESION
Issue Date
201112
Publisher
AMER SOC MICROBIOLOGY
Citation
INFECTION AND IMMUNITY, v.79, no.12, pp.4819 - 4827
Abstract
Pathogenic biofilms have been associated with persistent infections due to their high resistance to antimicrobial agents, while commensal biofilms often fortify the host's immune system. Hence, controlling biofilm formation of both pathogenic bacteria and commensal bacteria is important in bacterium-related diseases. We investigated the effect of plant flavonoids on biofilm formation of enterohemorrhagic Escherichia coli O157:H7. The antioxidant phloretin, which is abundant in apples, markedly reduced E. coli O157:H7 biofilm formation without affecting the growth of planktonic cells, while phloretin did not harm commensal E. coli K-12 biofilms. Also, phloretin reduced E. coli O157:H7 attachment to human colon epithelial cells. Global transcriptome analyses revealed that phloretin repressed toxin genes (hlyE and stx(2)), autoinducer-2 importer genes (lsrACDBF), curli genes (csgA and csgB), and dozens of prophage genes in E. coli O157:H7 biofilm cells. Electron microscopy confirmed that phloretin reduced fimbria production in E. coli O157:H7. Also, phloretin suppressed the tumor necrosis factor alpha-induced inflammatory response in vitro using human colonic epithelial cells. Moreover, in the rat model of colitis induced by trinitrobenzene sulfonic acid (TNBS), phloretin significantly ameliorated colon inflammation and body weight loss. Taken together, our results suggest that the antioxidant phloretin also acts as an inhibitor of E. coli O157:H7 biofilm formation as well as an anti-inflammatory agent in inflammatory bowel diseases without harming beneficial commensal E. coli biofilms.
URI
http://hdl.handle.net/YU.REPOSITORY/24181http://dx.doi.org/10.1128/IAI.05580-11
ISSN
0019-9567
Appears in Collections:
공과대학 > 화학공학부 > Articles
약학대학 > 약학부 > Articles
생명공학부 > 생명공학부 > Articles
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