Mesenchymal stem cell–gut microbiota interaction in the repair of inflammatory bowel disease: an enhanced therapeutic effect

Ocansey, Dickson Kofi Wiredu; Wang, Li; Wang, Jingyan; Yan, Yongmin; Qian, Hui; Zhang, Xu; Xu, Wenrong; Mao, Fei

doi:10.1186/s40169-019-0251-8

Clinical and Translational Medicine

Table 3 The influence of gut–bacteria on the functions of MSCs

From: Mesenchymal stem cell–gut microbiota interaction in the repair of inflammatory bowel disease: an enhanced therapeutic effect

Gut bacteria	Source of MSC	Experimental condition	Pathways/secretomes involved	Outcome of interaction	References
Specific-pathogen-free (SPF) gut microbiota	Bone marrow	DSS-induced colitis	Cell metabolic, HIF-1/inflammatory signaling, and neurodegenerative pathways	Altered MSC differentiation potential Enhanced immunomodulation capacity of MSC Decreased disease activity index	[67]
Lactobacillus acidophilus	Canine adipose	In vitro	Increased transcription of key immunomodulatory genes, like COX2, IL6 and IL8 Significantly increased PGE2	Enhanced immunoregulatory function No induction of MSC death, degeneration or diminished proliferation No effect on MSC migration	[70]
Salmonella typhi	Canine adipose	In vitro	Increased transcription of key immunomodulatory genes like COX2, IL6 and IL8	No induction of antigen-presenting phenotype Increased capacity of MSCs to inhibit mitogen-induced T-cell proliferation Induction and expression of PPARγ, IL-6, IL8, HGF, COX2, CD54 and PGE2 Impeded MSC migration	[70]
Restored composition and diversity of gut microbiota with Lactobacillus	Bone marrow	Chronic hypoxic rats	–	Restored defect of senescence, poor cell proliferation, cell cycle arrest and multi-lineage differentiation deficiency in MSCs Reduced d-galactose accumulation	[47]
Lactobacillus rhamnosus GG	Lamina propria of the villus	Intestinal radioprotection in vitro	TLR2 and COX-2 dependent induction	Lactobacillus rhamnosus GG produced LTA, which then primed the epithelial stem cell niche to protect epithelial stem cells by activating macrophages and PGE2 secreting MSCs	[76]
Helicobacter pylori	Bone marrow	GIT infection by H. pylori	Over-expression of TNFα and CCL2 TNFα leads to activation of NF-κB-dependent pathway	Stimulated migration of MSC	[77]

This presents a sum-up of documented impacts of gut microbiome including some pathogenic bacteria on the functions of MSCs. In each demonstration, certain functions of MSCs were mostly improved with no distortion to the inherent properties
PPARγ peroxisome proliferator activator receptor gamma, IL interleukin, HGF hepatocyte growth factor, COX2 cyclooxygenase 2, PGE2 prostaglandin 2, NF-κB Nuclear Factor-kappa B, TLR2 toll-like receptor 2, LTA lipoteichoic acid, CCL2 C–C motive Chemokine ligand 2, TNFα tumor necrosis factor α

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