Secretome of adipose derived-mesenchymal stem cells reduces the Vibrio cholerae attachment to Caco-2 cells and subsequent inflammatory responses

  • Alireza Moulazade Department of Immunology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran
  • Sara Soudi Department of Immunology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran
  • Bita Bakhshi Department of Bacteriology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran
Keywords: Inflammation; Apoptosis; Epithelium; Mesenchymal stem cell; Vibrio cholerae

Abstract

Background and Objectives: Mesenchymal Stem Cells (MSCs) can repair gastrointestinal tract damage. The Secretome of MSCs has a high capacity to inhibit bacterial colonization and the subsequent inflammatory responses of Vibrio cholerae. Materials and Methods: The Caco-2 cells were treated with adipose-derived MSCs (AD-MSCs) secretome and then in- fected with V. cholerae. Subsequently, the bacterial attachment and invasion, cholera toxin gene expression, PGE2 and IL-6 secretion, TNF-α, IL-1β, and IL-8 expression, and apoptosis of Caco-2 cells were evaluated.

Results: The secretome of AD-MSCs significantly reduced the V. cholerae attachment and internalization on Caco-2 epithe- lial cells (P<0.0001). The cholera toxin (Ctx-B) gene expression (FR=4.56 ± 0.66) and PGE2 production (P=0.0007) were also significantly reduced. The production of NO and TNF-α, IL-1β, and IL-8 pro-inflammatory cytokines were significantly (P<0.05) reduced in exposure to the secretome of AD-MSCs. Secretome also improved a significant 81.33% increase in IL-6 production (128.1 ± 37.6 pg/mL) and showed a 12.36% significant decrease in epithelial cell apoptosis (P< 0.0001) after exposure to V. cholerae.

Conclusion: The secretome of AD-MSCs can play a critical role in inhibiting bacterial colonization, and subsequent inflam- matory responses, and maintaining the integrity of the epithelial barrier. The secretome may be effective in the prevention of hypovolemic shock.

Published
2024-02-10
Section
Articles