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Lactobacillus acidophilus regulates STAT3 and STAT5 signaling in bovine β-lg-sensitized mice model

Abstract : AbstractOur previous study has shown that oral supplementation with Lactobacillus acidophilus KLDS 1.0738 could inhibit β-lactoglobulin (β-lg) allergy. In this study, we investigated the effect of L. acidophilus on the balance between T helper type 17 (Th17) cells and regulatory T cells (Treg) in allergic mouse model and explored the participation of related signal transducers and activator of transcription (STAT) in this process. Bovine β-lg-sensitized mice received strains KLDS 1.0738 for 3 weeks. After the allergen challenge, the percentages of Treg and Th17 cells, cytokine and STAT mRNA expression, and pSTAT protein levels were detected by flow cytometry, quantitative RT-PCR, and western blot, respectively. The results showed that stimulation with β-lg increased the levels of IL-6, pSTAT3, and Th17 cells, but decreased the levels of IL-2, pSTAT5, and Treg cells compared to the controls (P < 0.05). However, oral administration of L. acidophilus KLDS 1.0738 suppressed β-lg-induced inflammatory and improved the Treg/Th17 imbalance. In addition, L. acidophilus-treated group presented decrease in pSTAT3 activation, SOCS3, and IL-6 level, but increase in STAT5a/b, CD25, and IL-2 mRNA expression. These findings suggest that L. acidophilus could regulate IL-6/STAT3 and IL-2/STAT5 pathway, which may be responsible for the Treg/Th17 imbalance in β-lg-sensitized mice.
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Yun Zhang, Ai-Li Li, Yi-Qiao Sun, Peng Du, Li-Bo Liu, et al.. Lactobacillus acidophilus regulates STAT3 and STAT5 signaling in bovine β-lg-sensitized mice model. Dairy Science & Technology, EDP sciences/Springer, 2016, 96 (4), pp.501-512. ⟨10.1007/s13594-016-0284-3⟩. ⟨hal-01532436⟩



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