行業資訊 | 益生菌與免疫性肝炎
山西醫科大學：益生菌緩解小鼠自身免疫性肝炎
aluba
① 小鼠隨機分為4組：對照、AIH、AIH+益生菌（雙歧桿菌屬及擬桿菌屬的15個菌株）、AIH+地塞米松，干預42天；
② 益生菌及地塞米松均可抑制小鼠的炎癥細胞肝臟浸潤、血清轉氨酶水平、Th1及Th17細胞產生，但僅在益生菌組中觀察到Treg的增加；
③ 益生菌可維持小鼠的腸道屏障完整性，阻斷LPS的易位，抑制TLR4/NF-κB信號通路的活化，減少肝臟及回腸中的炎癥因子產生；
④ 益生菌可增加小鼠腸道菌群中的有益細菌的豐度，降低潛在有害細菌的豐度。
Probiotics alleviate autoimmune hepatitis in mice through modulation of gut microbiota and intestinal permeability
10.1016/j.jnutbio.2021.108863
【主編評語】自身免疫性肝炎（AIH）是一種免疫介導的慢性肝臟炎癥，伴隨著腸道菌群的失調。山西醫科大學的樊衛平團隊在Journal of Nutritional Biochemistry上發表的一項最新研究，發現益生菌可通過維持腸道屏障功能，抑制腸道LPS向肝臟的易位，以減少TLR4/NF-κB信號通路的活化，從而緩解AIH小鼠模型的肝臟炎癥。 （@aluba）
Probiotics alleviate autoimmune hepatitis in mice through modulation of gut microbiota and intestinal permeability
益生菌通過調節腸道菌群及腸道通透性緩解小鼠的自身免疫性肝炎
10.1016/j.jnutbio.2021.108863
2021-09-11, Article
Abstract:
Autoimmune hepatitis (AIH) is an immune-mediated type of chronic liver inflammation accompanied by intestinal flora imbalance. Probiotics have been reported to ameliorate imbalances in the intestinal flora. This study aimed to investigate the effects of compound probiotic in the AIH mouse model. AIH mice were gavaged with compound probiotic and injected intraperitoneally with dexamethasone (dex) for 42 days. The results showed that these treatments suppressed hepatic inflammatory cell infiltration, serum transaminase, and Th1 and Th17 cells. However, Treg cells were increased only in the probiotics group, which indicates an immunomodulatory role of the compound probiotic. The compound probiotic maintained intestinal barrier integrity, blocked lipopolysaccharide (LPS) translocation, and inhibited the activation of the TLR4/NF-κB pathway and the production of inflammatory factors in the liver and ileum. Moreover, the compound probiotic treatment increased the abundance of beneficial bacteria and reduced the abundance of potentially harmful bacteria in gut. Compound probiotic may improve ileal barrier function while increasing the diversity of the intestinal flora, blocking the translocation of gut-derived LPS to the liver and therefore preventing activation of the TLR4/NF-κB pathway. The resulting inhibition of pro-inflammatory factor production facilitates AIH remission.
First Authors:
Qingqing Liu
Correspondence Authors:
Weiping Fan
All Authors:
Qingqing Liu,Haixia Tian,Yongbo Kang,Yan Tian,Lin Li,Xing Kang,Hao Yang,Yanhong Wang,Jihua Tian,Fan Zhang,Mingwei Tong,Hongyan Cai,Weiping Fan
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