MatTek In Vitro Life Sciences Laboratories will be attending, exhibiting, and sponsoring a session at the tenth annual Advances in Cell and Tissue Culture conference. ACTC 2018 will be held at The School of Biosciences at Cardiff University from May 21st through May 23rd. MatTek IVLSL Senior Scientist and Production Manager, Dr. Jan Markus, will also be speaking and presenting at the conference. The talk will focus on MatTek’s EpiIntestinal tissue and its ability to model innate immune responses in the gut.
Modelling of Live Bacteria or Ligand-Induced Acute and Chronic Inflammation in the Gut using In Vitro 3D-Primary Reconstructed Human Small Intestinal Tissues (EpiIntestinal)
Speaker: Dr. Jan Markus, MatTek IVLSL Senior Scientist and Product Manager
Monday Afternoon Session, May 21st
Abstract: Intestinal epithelium is known to be involved in innate immune responses by recognizing potential pathogens through cellular pattern recognition receptors (PRRs). The purpose of this study was to investigate PRR responses following exposure of an in vitro reconstructed 3D human small intestinal (SMI) tissue to live bacteria or various Toll-like receptor (TLRs) and Node-like receptor (NOD) ligands. The SMI tissues are cultured using human intestinal fibroblasts and enterocytes and their 3-dimensional polarity and morphology mimic that of native in vivo tissues. Characterization of the SMI tissues included evaluation of structural features, barrier properties, and expression of drug transporters and drug metabolizing enzymes. Exposure of intestinal tissues to live bacterial (commensals and pathogens) or ligands to TLR4 (LPS) and NOD2 (Muramyl dipeptide; MDP) induced gene expression of pro-inflammatory cytokines such as IFN-β, IL-1β, IL-6, and RANTES. Prolonged exposure of intestinal tissues to IL-1β also resulted in reduced membrane integrity and induction of pro-inflammatory cytokines (IL-6 and CCL20) known to stimulate acquired immune cell responses by inducing cytokine release such as IL-17, TNF-α, and IFN-Ƴ or by initiating the migration of inflammatory cells. All these responses may be precursors to IBD-like disease. To simulate the effect of acquired immune cell responses on the intestinal epithelium, we also exposed the tissues to TNF-α and IFN- Ƴ, and IL-1 β, which compromised the barrier integrity and induced the release of pro-inflammatory cytokines. The effect of TNF-α and IFN- Ƴ on the intestinal epithelium was further exacerbated if antigen-presenting cells such as dendritic cells were incorporated into the 3D intestinal tissues.
In summary, our results suggest that the EpiIntestinal tissue is capable of modeling innate immune responses and can be a useful tool to study the complex interactions of human intestinal epithelium with microbiome in vitro.
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