Tytgat Institute for Liver and Intestinal Research, Academic Medical Center, University of Amsterdam, AMC, Amsterdam, The Netherlands.
BMC Gastroenterol. 2012 Apr 16;12:33. doi: 10.1186/1471-230X-12-33.
It is believed that inflammatory bowel diseases (IBD) result from an imbalance in the intestinal immune response towards the luminal microbiome. Dectin-1 is a widely expressed pattern recognition receptor that recognizes fungi and upon recognition it mediates cytokine responses and skewing of the adaptive immune system. Hence, dectin-1 may be involved in the pathogenesis of IBD.
We assessed the responses of dectin-1 deficient macrophages to the intestinal microbiota and determined the course of acute DSS and chronic Helicobacter hepaticus induced colitis in dectin-1 deficient mice.
We show that the mouse intestinal microbiota contains fungi and the cytokine responses towards this microbiota were significantly reduced in dectin-1 deficient macrophages. However, in two different colitis models no significant differences in the course of inflammation were found in dectin-1 deficient mice compared to wild type mice.
Together our data suggest that, although at the immune cell level there is a difference in response towards the intestinal flora in dectin-1 deficient macrophages, during intestinal inflammation this response seems to be redundant since dectin-1 deficiency in mice does not affect intestinal inflammation in experimental colitis.
人们认为炎症性肠病（IBD）是由于肠道免疫反应对腔微生物组失衡引起的。Dectin-1 是一种广泛表达的模式识别受体，可识别真菌，识别后可介导细胞因子反应和适应性免疫系统的偏斜。因此，dectin-1 可能参与 IBD 的发病机制。
我们评估了 dectin-1 缺陷型巨噬细胞对肠道微生物群的反应，并确定了急性 DSS 和慢性嗜肝螺杆菌诱导的结肠炎在 dectin-1 缺陷型小鼠中的病程。
我们表明，小鼠肠道微生物群中含有真菌，dectin-1 缺陷型巨噬细胞对这种微生物群的细胞因子反应明显降低。然而，在两种不同的结肠炎模型中，与野生型小鼠相比，dectin-1 缺陷型小鼠的炎症病程没有明显差异。
总之，我们的数据表明，尽管在免疫细胞水平上，dectin-1 缺陷型巨噬细胞对肠道菌群的反应存在差异，但在肠道炎症期间，这种反应似乎是多余的，因为小鼠中 dectin-1 的缺失并不影响实验性结肠炎中的肠道炎症。
