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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 bacteriaSource of MSCExperimental conditionPathways/secretomes involvedOutcome of interactionReferences
Specific-pathogen-free (SPF) gut microbiotaBone marrowDSS-induced colitisCell metabolic, HIF-1/inflammatory signaling, and neurodegenerative pathwaysAltered MSC differentiation potential
Enhanced immunomodulation capacity of MSC
Decreased disease activity index
Lactobacillus acidophilusCanine adiposeIn vitroIncreased 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
Salmonella typhiCanine adiposeIn vitroIncreased transcription of key immunomodulatory genes like COX2, IL6 and IL8No 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
Restored composition and diversity of gut microbiota with LactobacillusBone marrowChronic hypoxic ratsRestored defect of senescence, poor cell proliferation, cell cycle arrest and multi-lineage differentiation deficiency in MSCs
Reduced d-galactose accumulation
Lactobacillus rhamnosus GGLamina propria of the villusIntestinal radioprotection in vitroTLR2 and COX-2 dependent inductionLactobacillus 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 pyloriBone marrowGIT infection by H. pyloriOver-expression of TNFα and CCL2
TNFα leads to activation of NF-κB-dependent pathway
Stimulated migration of MSC[77]
  1. 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
  2. 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