Lactobacillus sakei K17, an inducer of IL-10 expression in antigen-presenting cells, attenuates TNBS-induced colitis in mice
Lactobacillus sakei K17, an inducer of IL-10 expression in antigen-presenting cells, attenuates TNBS-induced colitis in mice
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DOI：
10.1080/08923973.2016.1233981
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发表时间：
2016-12-01
影响因子：
3.3
通讯作者：
Kim, Dong-Hyun
中科院分区：
文献类型：
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作者：
Eun, Su-Hyeon;Lim, Su-Min;Kim, Dong-Hyun
为了了解上调树突状细胞（DC）和巨噬细胞中白细胞介素（IL）-10表达的益生菌的抗结肠炎作用，我们在从泡菜中收集的乳酸菌菌株中分离了在体外有效诱导DC和腹腔巨噬细胞中IL-10表达的清酒乳杆菌K17，并研究了其在具有2，4，6-三硝基苯磺酸（TNBS）诱导的结肠炎。在患有TNBS诱导的结肠炎的小鼠中口服K17（2x 10（9）CFU小鼠（-1）天（-1））抑制结肠缩短和髓过氧化物酶活性，以及CD 86（+）细胞向结肠中的浸润。用K17治疗还增加TNBS抑制的紧密连接蛋白和IL-10的表达，但抑制核因子-κ B（NF-B）和促分裂原活化蛋白激酶的活化以及肿瘤坏死因子和IL-17的表达。其作用与阳性市售抗结肠炎药柳氮磺胺吡啶（50 mg/kg）相当。此外，K17（1 × 10（5）CFU/mL）处理有效抑制了脂多糖（LPS）刺激的DC和腹腔巨噬细胞中的NF-B活化，并恢复了LPS刺激的Caco-2细胞中的紧密连接蛋白表达。这些结果表明，清酒乳杆菌K17可能通过上调IL-10和紧密连接蛋白的表达以及抑制NF-B活化来改善结肠炎。
To understand the anti-colitic effects of probiotics that up-regulate interleukin (IL)-10 expression in dendritic cells (DCs) and macrophages, we isolated Lactobacillus sakei K17, which potently induced IL-10 expression in DCs and peritoneal macrophages in vitro, among the lactic acid bacteria strains collected from kimchi and investigated its anti-inflammatory effect in mice with 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis. Oral administration of K17 (2x10(9) CFUmouse(-1)day(-1)) in mice with TNBS-induced colitis suppressed colon shortening and myeloperoxidase activity, as well as infiltration of CD86(+)cells into the colon. Treatment with K17 also increased TNBS-suppressed expression of tight junction proteins and IL-10, but inhibited activation of nuclear factor-kappaB (NF-B) and mitogen-activated protein kinases and expression of tumor necrosis factor and IL-17. Its effect was comparable with that of sulfasalazine (50mg/kg), a positive commercial ant-colitic drug. Furthermore, treatment with K17 (1x10(5) CFU/mL) potently inhibited lipopolysaccharide (LPS)-stimulated NF-B activation in DCs and peritoneal macrophages and restored tight junction protein expression in LPS-stimulated Caco-2 cells. These findings suggest that Lactobacillus sakei K17 may ameliorate colitis by up-regulating the expression of IL-10 and tight junction proteins and inhibiting NF-B activation.