Microorganisms (Apr 2024)

Cell-Free Culture Supernatant of <i>Lactobacillus acidophilus</i> AG01 and <i>Bifidobacterium animalis</i> subsp. <i>lactis</i> AG02 Reduces the Pathogenicity of NetB-Positive <i>Clostridium perfringens</i> in a Chicken Intestinal Epithelial Cell Line

  • Darshana Kadekar,
  • Andreea Cornelia Udrea,
  • Steffen Yde Bak,
  • Niels Christensen,
  • Kirsty Gibbs,
  • Chong Shen,
  • Marion Bernardeau

DOI
https://doi.org/10.3390/microorganisms12040839
Journal volume & issue
Vol. 12, no. 4
p. 839

Abstract

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The worldwide reduction in the use of antibiotics in animal feed is fueling the need for alternatives for the prevention and control of poultry intestinal diseases such as necrotic enteritis (NE), which is caused by Clostridium perfringens. This is the first report on the use of an intestinal epithelial chicken cell line (CHIC-8E11) to study the pathogenic traits of C. perfringens and to investigate the mode of action of cell-free supernatants (CFS) from probiotic Lactobacillus acidophilus AG01 and Bifidobacterium animalis subsp. lactis AG02 in reducing the pathogenicity of C. perfringens. The cell adhesion, permeability and cytotoxicity were assessed under challenge with four C. perfringens strains isolated from broiler NE episodes of differing geographical origin (CP1–UK; CP10–Sweden; 25037–CP01 and CP22–USA). All the C. perfringens strains could adhere to the CHIC-8E11 cells, with varying affinity (0.05–0.48% adhesion across the strains). The CFS from one out of two strains (CP22) increased the cell permeability (+4.5-fold vs. the control, p B. animalis subsp. lactis AG02 but not L. acidophilus AG01 reduced the cell adhesion of three out of four C. perfringens strains (by 77–85% vs. the control, p C. perfringens strains, which was dependent on the dose. The results confirm the suitability of the CHIC-8E11 cell line for the study of host–pathogen cell interactions in the context of NE caused by C. perfringens and reveal a beneficial mode of action of B. animalis subsp. lactis AG02 in reducing C. perfringens cell adhesion and, together with L. acidophilus AG01, in reducing C. perfringens cytotoxicity.

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