Ma He, Mueed Abdul, Ma Yanxu, Ibrahim Muhammad, Su Ling, Wang Qi
Engineering Research Center of Chinese Ministry of Education for Edible and Medicinal Fungi, Jilin Agricultural University, Changchun 130118, China.
College of Plant Protection, Jilin Agricultural University, Changchun 130012, China.
Foods. 2024 Nov 30;13(23):3881. doi: 10.3390/foods13233881.
polysaccharides (FLP1s) have potential biological activities. Our previous study showed that FLP1s positively regulated gut immunity and microbiota. However, it is still unclear whether FLP1s mediate gut microbiota in immunosuppressed mice. This research aims to explore the relationship between FLP1-mediated gut microbes and intestinal immunity in immunosuppressed mice through fecal microbiota transplantation (FMT). The results demonstrated that FLP1s exhibited prebiotic and anti-immunosuppressive effects on CTX-induced immunosuppressed mice. FFLP1 treatment (microbiota transplantation from the fecal sample) remarkably elevated the production of sIgA and secretion of the anti-inflammatory cytokines IL-4, TNF-α, and IFN-γ in the intestine of CTX-treated mice, inducing activation of the MAPK pathway. Moreover, FFLP1s mitigated oxidative stress by activating the Nrf2/Keap1 signaling pathway and strengthened the intestinal barrier function by upregulating the expression level of tight junction proteins (occludin, claudin-1, MUC-2, and ZO-1). Furthermore, FFPL1s restored gut dysbiosis in CTX-treated immunosuppressed mice by increasing the abundance of , , and . They also modified the composition of fecal metabolites, leading to enhanced regulation of lipolysis in adipocytes, the cGMP-PKG pathway, the Rap1 signaling pathway, and ovarian steroidogenesis, as indicated by KEGG pathway analysis. These findings indicate that FLP1s could modulate the response of the intestinal immune system through regulation of the gut microbiota, thus promoting immune activation in CTX-treated immunosuppressed mice. FLP1s can serve as a natural protective agent against CTX-induced immune injury.
多糖（FLP1s）具有潜在的生物活性。我们之前的研究表明，FLP1s对肠道免疫和微生物群具有正向调节作用。然而，FLP1s是否介导免疫抑制小鼠的肠道微生物群仍不清楚。本研究旨在通过粪便微生物群移植（FMT）探索免疫抑制小鼠中FLP1介导的肠道微生物与肠道免疫之间的关系。结果表明，FLP1s对环磷酰胺（CTX）诱导的免疫抑制小鼠具有益生元和抗免疫抑制作用。FFLP1处理（从粪便样本中进行微生物群移植）显著提高了CTX处理小鼠肠道中分泌型免疫球蛋白A（sIgA）的产生以及抗炎细胞因子白细胞介素-4（IL-4）、肿瘤坏死因子-α（TNF-α）和干扰素-γ（IFN-γ）的分泌，诱导丝裂原活化蛋白激酶（MAPK）途径的激活。此外，FFLP1s通过激活核因子E2相关因子2/ Kelch样环氧氯丙烷相关蛋白1（Nrf2/Keap1）信号通路减轻氧化应激，并通过上调紧密连接蛋白（闭合蛋白、claudin-1、黏蛋白-2和紧密连接蛋白-1）的表达水平增强肠道屏障功能。此外，FFPL1s通过增加 、 和 的丰度恢复了CTX处理的免疫抑制小鼠的肠道菌群失调。KEGG通路分析表明，它们还改变了粪便代谢物的组成，导致脂肪细胞中脂解、环磷酸鸟苷-蛋白激酶G（cGMP-PKG）途径、Rap1信号通路和卵巢类固醇生成的调节增强。这些发现表明，FLP1s可以通过调节肠道微生物群来调节肠道免疫系统的反应，从而促进CTX处理的免疫抑制小鼠的免疫激活。FLP1s可作为一种天然保护剂，抵抗CTX诱导的免疫损伤。
