Rodenburg Wendy, Keijer Jaap, Kramer Evelien, Roosing Susanne, Vink Carolien, Katan Martijn B, van der Meer Roelof, Bovee-Oudenhoven Ingeborg M J
TI Food and Nutrition, PO Box 557, 6700 AN, Wageningen, The Netherlands.
BMC Microbiol. 2007 Sep 12;7:84. doi: 10.1186/1471-2180-7-84.
Salmonella enteritidis is suggested to translocate in the small intestine. In vivo it induces gene expression changes in the ileal mucosa and Peyer's patches. Stimulation of Salmonella translocation by dietary prebiotics fermented in colon suggests involvement of the colon as well. However, effects of Salmonella on colonic gene expression in vivo are largely unknown. We aimed to characterize time dependent Salmonella-induced changes of colonic mucosal gene expression in rats using whole genome microarrays. For this, rats were orally infected with Salmonella enteritidis to mimic a foodborne infection and colonic gene expression was determined at days 1, 3 and 6 post-infection (n = 8 rats per time-point). As fructo-oligosaccharides (FOS) affect colonic physiology, we analyzed colonic mucosal gene expression of FOS-fed versus cellulose-fed rats infected with Salmonella in a separate experiment. Colonic mucosal samples were isolated at day 2 post-infection.
Salmonella affected transport (e.g. Chloride channel calcium activated 6, H+/K+ transporting Atp-ase), antimicrobial defense (e.g. Lipopolysaccharide binding protein, Defensin 5 and phospholipase A2), inflammation (e.g. calprotectin), oxidative stress related genes (e.g. Dual oxidase 2 and Glutathione peroxidase 2) and Proteolysis (e.g. Ubiquitin D and Proteosome subunit beta type 9). Furthermore, Salmonella translocation increased serum IFN gamma and many interferon-related genes in colonic mucosa. The gene most strongly induced by Salmonella infection was Pancreatitis Associated Protein (Pap), showing >100-fold induction at day 6 after oral infection. Results were confirmed by Q-PCR in individual rats. Stimulation of Salmonella translocation by dietary FOS was accompanied by enhancement of the Salmonella-induced mucosal processes, not by induction of other processes.
We conclude that the colon is a target tissue for Salmonella, considering the abundant changes in mucosal gene expression.
肠炎沙门氏菌被认为可在小肠内移位。在体内，它会诱导回肠黏膜和派尔集合淋巴结中的基因表达发生变化。结肠中发酵的膳食益生元对沙门氏菌移位的刺激表明结肠也参与其中。然而，沙门氏菌对体内结肠基因表达的影响在很大程度上尚不清楚。我们旨在使用全基因组微阵列来表征大鼠体内沙门氏菌诱导的结肠黏膜基因表达的时间依赖性变化。为此，给大鼠口服肠炎沙门氏菌以模拟食源性感染，并在感染后第1、3和6天测定结肠基因表达（每个时间点n = 8只大鼠）。由于低聚果糖（FOS）会影响结肠生理，我们在另一个实验中分析了喂食FOS与喂食纤维素的感染沙门氏菌大鼠的结肠黏膜基因表达。在感染后第2天分离结肠黏膜样本。
沙门氏菌影响转运（如氯离子通道钙激活蛋白6、H+/K+转运ATP酶）、抗菌防御（如脂多糖结合蛋白、防御素5和磷脂酶A2）、炎症（如钙卫蛋白）、氧化应激相关基因（如双氧化酶2和谷胱甘肽过氧化物酶2）以及蛋白水解（如泛素D和蛋白酶体亚基β9型）。此外，沙门氏菌移位增加了血清干扰素γ以及结肠黏膜中许多与干扰素相关的基因。沙门氏菌感染诱导最强的基因是胰腺炎相关蛋白（Pap），口服感染后第6天诱导倍数超过100倍。在个体大鼠中通过定量聚合酶链反应（Q-PCR）证实了结果。膳食FOS对沙门氏菌移位的刺激伴随着沙门氏菌诱导的黏膜过程的增强，而非其他过程的诱导。
考虑到黏膜基因表达的大量变化，我们得出结论，结肠是沙门氏菌的靶组织。
