Multiple effects of Escherichia coli Nissle 1917 on growth, biofilm formation, and inflammation cytokines profile of Clostridium perfringens type A strain CP4

Yanlong Jiang, Qingke Kong, Kenneth L. Roland, Amanda Wolf, Roy Curtiss

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

Clostridium perfringens is an important Gram-positive pathogen responsible for food poisoning, necrotic enteritis, gas gangrene, and even death. Escherichia coli Nissle 1917 (EcN) is a well-characterized probiotic strain with demonstrated benefits. In this study, we evaluated the effects of EcN on growth, toxin production, biofilm formation, and inflammatory cytokine responses of C. perfringens. In vitro co-culture experiments demonstrated that EcN inhibited growth, gas production, and toxin production (α-toxin and NetB) of C. perfringens in a dose-dependent manner. The growth inhibition effect was not observed when C. perfringens was incubated with EcN cell-free supernatants (CFS<inf>E</inf>), suggesting that growth inhibition was caused by nutrition competition during co-incubation. In vitro studies demonstrated that pre-incubation with EcN did not inhibit C. perfringens attachment to Caco-2 cells, but did reduce C. perfringens total number, toxin production, and cytotoxicity after 24 h. The similar growth inhibition results were also observed during the formation of C. perfringens biofilm. Finally, pre-incubation of EcN with RAW264.7 cells significantly decreased the production of inflammatory cytokines caused by the introduction of C. perfringens. Our results indicate that EcN can inhibit many of the pathological effects of C. perfringens in vitro conditions.

Original languageEnglish (US)
Pages (from-to)390-400
Number of pages11
JournalPathogens and Disease
Volume70
Issue number3
DOIs
StatePublished - 2014

Fingerprint

Clostridium perfringens
Biofilms
Cytokines
Escherichia coli
Inflammation
Growth
Gas Gangrene
Foodborne Diseases
Caco-2 Cells
Enteritis
Probiotics
Coculture Techniques
Gases

Keywords

  • Biofilm
  • C. perfringens
  • Cytokine
  • E. coli Nissle 1917
  • Inhibition
  • Toxin

ASJC Scopus subject areas

  • Immunology and Allergy
  • Infectious Diseases
  • Microbiology (medical)
  • Immunology and Microbiology(all)
  • Medicine(all)

Cite this

Multiple effects of Escherichia coli Nissle 1917 on growth, biofilm formation, and inflammation cytokines profile of Clostridium perfringens type A strain CP4. / Jiang, Yanlong; Kong, Qingke; Roland, Kenneth L.; Wolf, Amanda; Curtiss, Roy.

In: Pathogens and Disease, Vol. 70, No. 3, 2014, p. 390-400.

Research output: Contribution to journalArticle

Jiang, Yanlong ; Kong, Qingke ; Roland, Kenneth L. ; Wolf, Amanda ; Curtiss, Roy. / Multiple effects of Escherichia coli Nissle 1917 on growth, biofilm formation, and inflammation cytokines profile of Clostridium perfringens type A strain CP4. In: Pathogens and Disease. 2014 ; Vol. 70, No. 3. pp. 390-400.
@article{8437d5d57cd84d80b874f97e54f25ccd,
title = "Multiple effects of Escherichia coli Nissle 1917 on growth, biofilm formation, and inflammation cytokines profile of Clostridium perfringens type A strain CP4",
abstract = "Clostridium perfringens is an important Gram-positive pathogen responsible for food poisoning, necrotic enteritis, gas gangrene, and even death. Escherichia coli Nissle 1917 (EcN) is a well-characterized probiotic strain with demonstrated benefits. In this study, we evaluated the effects of EcN on growth, toxin production, biofilm formation, and inflammatory cytokine responses of C. perfringens. In vitro co-culture experiments demonstrated that EcN inhibited growth, gas production, and toxin production (α-toxin and NetB) of C. perfringens in a dose-dependent manner. The growth inhibition effect was not observed when C. perfringens was incubated with EcN cell-free supernatants (CFSE), suggesting that growth inhibition was caused by nutrition competition during co-incubation. In vitro studies demonstrated that pre-incubation with EcN did not inhibit C. perfringens attachment to Caco-2 cells, but did reduce C. perfringens total number, toxin production, and cytotoxicity after 24 h. The similar growth inhibition results were also observed during the formation of C. perfringens biofilm. Finally, pre-incubation of EcN with RAW264.7 cells significantly decreased the production of inflammatory cytokines caused by the introduction of C. perfringens. Our results indicate that EcN can inhibit many of the pathological effects of C. perfringens in vitro conditions.",
keywords = "Biofilm, C. perfringens, Cytokine, E. coli Nissle 1917, Inhibition, Toxin",
author = "Yanlong Jiang and Qingke Kong and Roland, {Kenneth L.} and Amanda Wolf and Roy Curtiss",
year = "2014",
doi = "10.1111/2049-632X.12153",
language = "English (US)",
volume = "70",
pages = "390--400",
journal = "Pathogens and Disease",
issn = "2049-632X",
publisher = "John Wiley & Sons Inc.",
number = "3",

}

TY - JOUR

T1 - Multiple effects of Escherichia coli Nissle 1917 on growth, biofilm formation, and inflammation cytokines profile of Clostridium perfringens type A strain CP4

AU - Jiang, Yanlong

AU - Kong, Qingke

AU - Roland, Kenneth L.

AU - Wolf, Amanda

AU - Curtiss, Roy

PY - 2014

Y1 - 2014

N2 - Clostridium perfringens is an important Gram-positive pathogen responsible for food poisoning, necrotic enteritis, gas gangrene, and even death. Escherichia coli Nissle 1917 (EcN) is a well-characterized probiotic strain with demonstrated benefits. In this study, we evaluated the effects of EcN on growth, toxin production, biofilm formation, and inflammatory cytokine responses of C. perfringens. In vitro co-culture experiments demonstrated that EcN inhibited growth, gas production, and toxin production (α-toxin and NetB) of C. perfringens in a dose-dependent manner. The growth inhibition effect was not observed when C. perfringens was incubated with EcN cell-free supernatants (CFSE), suggesting that growth inhibition was caused by nutrition competition during co-incubation. In vitro studies demonstrated that pre-incubation with EcN did not inhibit C. perfringens attachment to Caco-2 cells, but did reduce C. perfringens total number, toxin production, and cytotoxicity after 24 h. The similar growth inhibition results were also observed during the formation of C. perfringens biofilm. Finally, pre-incubation of EcN with RAW264.7 cells significantly decreased the production of inflammatory cytokines caused by the introduction of C. perfringens. Our results indicate that EcN can inhibit many of the pathological effects of C. perfringens in vitro conditions.

AB - Clostridium perfringens is an important Gram-positive pathogen responsible for food poisoning, necrotic enteritis, gas gangrene, and even death. Escherichia coli Nissle 1917 (EcN) is a well-characterized probiotic strain with demonstrated benefits. In this study, we evaluated the effects of EcN on growth, toxin production, biofilm formation, and inflammatory cytokine responses of C. perfringens. In vitro co-culture experiments demonstrated that EcN inhibited growth, gas production, and toxin production (α-toxin and NetB) of C. perfringens in a dose-dependent manner. The growth inhibition effect was not observed when C. perfringens was incubated with EcN cell-free supernatants (CFSE), suggesting that growth inhibition was caused by nutrition competition during co-incubation. In vitro studies demonstrated that pre-incubation with EcN did not inhibit C. perfringens attachment to Caco-2 cells, but did reduce C. perfringens total number, toxin production, and cytotoxicity after 24 h. The similar growth inhibition results were also observed during the formation of C. perfringens biofilm. Finally, pre-incubation of EcN with RAW264.7 cells significantly decreased the production of inflammatory cytokines caused by the introduction of C. perfringens. Our results indicate that EcN can inhibit many of the pathological effects of C. perfringens in vitro conditions.

KW - Biofilm

KW - C. perfringens

KW - Cytokine

KW - E. coli Nissle 1917

KW - Inhibition

KW - Toxin

UR - http://www.scopus.com/inward/record.url?scp=84921286254&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84921286254&partnerID=8YFLogxK

U2 - 10.1111/2049-632X.12153

DO - 10.1111/2049-632X.12153

M3 - Article

C2 - 24532573

AN - SCOPUS:84921286254

VL - 70

SP - 390

EP - 400

JO - Pathogens and Disease

JF - Pathogens and Disease

SN - 2049-632X

IS - 3

ER -