Skip to main navigation Skip to search Skip to main content

Exploring host-commensal-pathogen dynamics in cell line and organotypic human intestinal epithelial models

  • National Institute of Public Health and the Environment
  • Laboratory of Medical Immunology
  • Department of Radiology, Amsterdam UMC the Netherlands.

Research output: Contribution to journal › Article › Academic › peer-review

47 Downloads (Pure)

Abstract

Host and microbiome intricately interact in the ecosystem of the human digestive tract, playing a crucial role in our health. These interactions can initiate immune responses in the epithelial cells, which, in turn, activate downstream responses in other immune cells. Here, we used a CaCo-2 and a human intestinal enteroid (HIE) model to explore epithelial responses to both commensal and pathogenic bacteria, individually and combined. CaCo-2 cells were co-cultured with peripheral blood mononuclear cells, revealing downstream activation of immune cells. While both systems showed comparable cytokine profiles, they differed in their responses to the different bacteria, with the organoid system being more representative of responses observed in humans. We provide evidence of the pro-inflammatory responses associated with these bacteria. These models contribute to a deeper understanding of the interactions between the microbiota, intestinal epithelium, and immune cells in the gut, promoting advances in the field of host-microbe interactions.
Original languageEnglish
Article number109771
JournaliScience
Volume27
Issue number5
DOIs
Publication statusPublished - 17 May 2024

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

  1. SDG 3 - Good Health and Well-being
    SDG 3 Good Health and Well-being

Keywords

  • Cell biology
  • Microbiology
  • Microbiome

Fingerprint

Dive into the research topics of 'Exploring host-commensal-pathogen dynamics in cell line and organotypic human intestinal epithelial models'. Together they form a unique fingerprint.

Cite this