Department of Human Biology, Maastricht University Medical Centre+, NUTRIM School for Nutrition, Toxicology and Metabolism, Maastricht, The Netherlands.
Nutr Res. 2010 Jan;30(1):40-8. doi: 10.1016/j.nutres.2009.10.023.
Dietary components, like beta-glucans, can modulate the intestinal immune response. We previously showed that fecal water enriched with oat beta-glucan stimulated the cytokine-induced immune response of enterocytes. It is, however, unclear whether beta-glucans activate nuclear factor-kappaB (NF-kappaB) pathways in the intestine in vivo and if so, whether enterocytes, intestinal leukocytes, or both respond to beta-glucans. We evaluated the effects of an oral gavage of 3 mg dietary oat (1-->3), (1-->4)-beta-D-glucans that was administered twice daily during 3.5 days on intestinal NF-kappaB transactivation and subsequent cytokine production of intestinal leukocytes and enterocytes in 16 NF-kappaB reporter mice. We hypothesized that oat beta-glucan activates the central immune transcription factor NF-kappaB and increased cytokine secretion, as we previously reported immune stimulating effects by oat beta-glucan. We found that mice that were administered oat beta-glucans (n = 8) showed an increased intestinal NF-kappaB transactivation in leukocytes (P = .021) and enterocytes (P = .012), particularly in the proximal part of the small intestine (ileum), as compared to placebo mice (n = 8). Surprisingly, NF-kappaB was not activated in the colon. Furthermore, the level of interleukin 12 was increased in intestinal lysates from all compartments, whereas the concentration of interferon gamma was decreased in the proximal small intestine (P = .046). Finally, tumor necrosis factor alpha showed a trend toward a reduced production in the colon (P = .057). Because we have earlier shown that human enterocyte cell lines do not express the beta-glucan receptor dectin-1 in vitro, we now conclude that after consumption, dietary oat beta-glucans most likely firstly activate the intestinal leukocytes, which in turn increases cellular activation of enterocytes.
膳食成分,如β-葡聚糖,可以调节肠道免疫反应。我们之前的研究表明,富含燕麦β-葡聚糖的粪便水可刺激肠细胞的细胞因子诱导免疫反应。然而,目前尚不清楚β-葡聚糖是否在体内激活肠道核因子-κB(NF-κB)途径,如果是这样,β-葡聚糖是激活肠细胞、肠道白细胞还是两者。我们评估了在 16 只 NF-κB 报告小鼠中,每天两次口服 3mg 膳食燕麦(1-->3),(1-->4)-β-D-葡聚糖,连续 3.5 天,对肠道 NF-κB 转激活和随后肠道白细胞和肠细胞细胞因子产生的影响。我们假设燕麦β-葡聚糖激活了中央免疫转录因子 NF-κB,并增加了细胞因子的分泌,正如我们之前报道的燕麦β-葡聚糖具有免疫刺激作用。我们发现,给予燕麦β-葡聚糖的小鼠(n=8)与安慰剂小鼠(n=8)相比,白细胞(P=0.021)和肠细胞(P=0.012)的肠道 NF-κB 转激活增加,特别是在小肠近端(回肠)。令人惊讶的是,NF-κB 在结肠中没有被激活。此外,所有部位的肠匀浆中白细胞介素 12 水平升高,而近端小肠(P=0.046)中干扰素γ浓度降低。最后,肿瘤坏死因子-α在结肠中显示出产生减少的趋势(P=0.057)。因为我们之前已经表明,人肠细胞系在体外不表达β-葡聚糖受体 dectin-1,所以我们现在得出结论,摄入膳食燕麦β-葡聚糖后,它很可能首先激活肠道白细胞,进而增加肠细胞的细胞活化。