4.7 Article

Modulation of intestinal epithelial cell proliferation and apoptosis by Lactobacillus gasseri SF1183

Journal

SCIENTIFIC REPORTS
Volume 12, Issue 1, Pages -

Publisher

NATURE PORTFOLIO
DOI: 10.1038/s41598-022-24483-0

Keywords

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Funding

  1. University of Naples of Federico II (Funds MUR Ministero Universita Ricerca FRA Finanziamento della Ricerca di Ateneo)
  2. Department Research Funds

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The gut microbiota plays a positive role in maintaining intestinal homeostasis through various mechanisms. This study investigated the effects of molecules secreted by Lactobacillus gasseri SF1183 on HCT116 cells and found that these molecules can reversibly reduce cell proliferation and protect cells from apoptosis. Additionally, they enhance the barrier function between cells.
The gut microbiota exerts a variety of positive effects on the intestinal homeostasis, including the production of beneficial molecules, control of the epithelial barrier integrity and the regulation of the balance between host's cell death and proliferation. The interactions between commensal bacteria and intestinal cells are still under-investigated and is then of paramount importance to address such interactions at the molecular and cellular levels. We report an in vitro analysis of the effects of molecules secreted by Lactobacillus gasseri SF1183 on HCT116 cells, selected as a model of intestinal epithelial cells. SF1183 is a L. gasseri strain isolated from an ileal biopsy of a human healthy volunteer, able to prevent colitis symptoms in vivo. Expanding previous findings, we show that bioactive molecules secreted by SF1183 reduce the proliferation of HCT116 cells in a reversible manner determining a variation in cell cycle markers (p21WAF, p53, cyclin D1) and resulting in the protection of HCT116 cells from TNF-alfa induced apoptosis, an effect potentially relevant for the protection of the epithelial barrier integrity and reconstitution of tissue homeostasis. Consistently, SF1183 secreted molecules increase the recruitment of occludin, a major component of TJ, at the cell-cell contacts, suggesting a reinforcement of the barrier function.

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