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2'-Fucosyllactose Inhibits Imiquimod-Induced Psoriasis in Mice By Regulating Th17 Cell Response Via The Stat 3 Signaling Pathway

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2 Fucosyllactose Inhibits Imiquimod Induced Psoriasis In Mice By Regulating Th17 Cell Response Via The Stat3 Signaling Pathway 2 Fucosyllactose Inhibits Imiquimod Induced Psoriasis In Mice By Regulating Th17 Cell Response Via The Stat3 Signaling Pathway
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  • HMO: 2´-FUCOSYLLACTOSE (2’-FL)
  • Human Milk Oligosaccharides (HMO)
  • Prebiotics
  • Psoriasis is a chronic immune-mediated inflammatory cutaneous disorder with Th17 cells and Th17-related cytokines playing an important role in its development. 2′-FL (2′-fucosyllactose), which makes up about 30% of all HMOs (human milk oligosaccharides) in blood type secretor positive maternal milk, plays an essential role in supporting aspects of immune development and regulation.
  • To explore the immunomodulatory effect of 2′-FL in psoriasis, we employed the imiquimod (IMQ)-induced psoriasis-like mouse model. Our data showed that mice administered with 2′-FL exhibited attenuated skin damage and inflammation, characterized by significantly decreased erythema and thickness and reduced recruitment of pro-inflammatory cytokines when compared to control mice.
  • The alleviated skin inflammation in 2′-FL treated mice was associated with a reduced proportion of Th17 cells and decreased production of Th17-related cytokines. Furthermore, we have demonstrated that 2′-FLreduced the phosphorylation of STAT3 in the skin tissue from mice with IMQ stimulation, which could account for the decreasing recruitment of Th17 cells. In vitro studies showed that 2′-FL inhibited differentiation of Th17cells, phosphorylation of STAT3, and RORγt mRNA levels in T cells under Th17 polarization.
  • Our results indicate that 2′-FL ameliorates IMQ-induced psoriasis by inhibiting Th17 cell immune response and Th17-related cytokine secretion via modulation of the STAT3 signaling pathway.
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Biostime Institute for Nutrition and Care
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