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Amelioration of colitis in mice by Leuconostoc lactis EJ-1 by M1 to M2 macrophage polarization.
Microbiology and Immunology ( IF 1.9 ) Pub Date : 2019-11-15 , DOI: 10.1111/1348-0421.12752
Se-Eun Jang 1 , Sung-Won Min 2
Affiliation  

Dysregulation of immune responses to environmental antigens by the intestine leads to the chronic inflammatory disease, inflammatory bowel disease (IBD). Recent studies have thus sought to identify a dietary component that can inhibit lipopolysaccharide (LPS)-induced nuclear factor-kappa beta (NF-κB) signaling to ameliorate IBD. This study assessed if the lactic acid bacteria (LAB) from kimchi, suppresses the expression of tumor necrosis factor-alpha (TNF-α) in peritoneal macrophages induced by LPS. Leuconostoc lactis EJ-1, an isolate from LAB, reduced the expression of interleukin-6 (IL-6) and IL-1β in peritoneal macrophages induced by LPS. The study further tested whether EJ-1 alleviates colitis induced by 2,4,6-trinitrobenzene sulfonic acid (TNBS) in mice. TNBS significantly increased myeloperoxidase (MPO) expression, macroscopic colitis scores, and colon shortening. Oral administration of L. lactis EJ-1 resulted in an inhibited in TNBS-induced loss in body weight, colon shortening, MPO activity, and NF-κB and inducible nitric oxide synthase expression; it also led to a marked reduction in cyclooxygenase-2 expression. L. lactis EJ-1 also inhibited the TNBS-induced expression of TNF-α, IL-1β, and IL-6; however, it induced the expression of IL-10. The M2 macrophage markers arginase I, IL-10, and CD206 were elevated by EJ-1. Collectively, these results suggest that EJ-1 inhibits the NF-κB signaling and polarizes M1- to M2-macrophage transition, which help in ameliorating colitis.

中文翻译:

M1至M2巨噬细胞极化对乳酸乳球菌EJ-1对小鼠结肠炎的缓解作用。

肠道对环境抗原的免疫反应失调会导致慢性炎症性疾病,即炎症性肠病(IBD)。因此,最近的研究试图确定一种饮食成分,该成分可以抑制脂多糖(LPS)诱导的核因子-κβ(NF-κB)信号,从而改善IBD。这项研究评估了泡菜中的乳酸菌(LAB)是否能抑制LPS诱导的腹膜巨噬细胞中肿瘤坏死因子-α(TNF-α)的表达。来自乳酸菌的一种分离乳酸乳球菌EJ-1,可降低LPS诱导的腹膜巨噬细胞中白介素6(IL-6)和IL-1β的表达。该研究进一步测试了EJ-1是否能减轻小鼠2,4,6-三硝基苯磺酸(TNBS)诱发的结肠炎。TNBS显着增加了髓过氧化物酶(MPO)的表达,宏观结肠炎评分,和结肠缩短。口服乳酸乳球菌EJ-1可抑制TNBS诱导的体重减轻,结肠缩短,MPO活性和NF-κB以及诱导型一氧化氮合酶的表达。它也导致环氧合酶2表达的显着降低。乳酸乳球菌EJ-1也抑制TNBS诱导的TNF-α,IL-1β和IL-6的表达。然而,它诱导IL-10的表达。EJ-1使M2巨噬细胞标记精氨酸酶I,IL-10和CD206升高。总的来说,这些结果表明,EJ-1抑制NF-κB信号传导并使M1到M2巨噬细胞的转变极化,这有助于缓解结肠炎。它也导致环氧合酶2表达的显着降低。乳酸乳球菌EJ-1也抑制TNBS诱导的TNF-α,IL-1β和IL-6的表达。然而,它诱导IL-10的表达。EJ-1使M2巨噬细胞标记精氨酸酶I,IL-10和CD206升高。总的来说,这些结果表明,EJ-1抑制NF-κB信号传导并使M1到M2巨噬细胞的转变极化,这有助于缓解结肠炎。它也导致环氧合酶2表达的显着降低。乳酸乳球菌EJ-1也抑制TNBS诱导的TNF-α,IL-1β和IL-6的表达。然而,它诱导IL-10的表达。EJ-1使M2巨噬细胞标记精氨酸酶I,IL-10和CD206升高。总的来说,这些结果表明,EJ-1抑制NF-κB信号传导并使M1到M2巨噬细胞的转变极化,这有助于缓解结肠炎。
更新日期:2019-11-01
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