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Bacterial Overgrowth in the Cystic Fibrosis Transmembrane Conductance Regulator Null Mouse Small Intestine

机译：细菌在囊性纤维化跨膜电导调节剂无效小鼠小肠中的过度生长。

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We recently reported the inflammation of the cystic fibrosis (CF) mouse small intestine, and we hypothesized bacterial overgrowth as a possible cause. Quantitative PCR of bacterial 16S genomic DNA in the CF mouse small intestine revealed an increase of greater than 40-fold compared to controls. Sequencing of 16S PCR products and Gram staining showed that the majority of bacteria in the CF mouse intestine were gram negative. Bacteria were observed to colonize the mucus that accumulates in the intestinal lumen of mice with CF. Impaired Paneth cell defenses were suggested by observation of partially dispersed Paneth granules in the mucus plugs of CF mouse intestinal crypts, and this mucus was strongly immunoreactive for Paneth cell bactericidal products. The role of bacterial overgrowth in intestinal inflammation in CF was tested by treating mice with oral antibiotics (ciprofloxacin and metronidazole) for 3 weeks, which reduced bacterial load in the CF mouse small intestine over 400-fold. Antibiotic treatment decreased the expression of the inflammation-related genes mast cell protease 2, leucine-rich α2 glycoprotein/leucine-rich high endothelial venule glycoprotein, suppressor of cytokine signaling 3, hematopoietic cell transcript 1, and resistin-like molecule β/found in inflammatory zone 2, all of which were no longer expressed at levels significantly different from control levels. The reduction of intestinal bacteria also significantly improved the growth of CF mice but had no effect on the growth of wild-type mice. These data suggest that bacterial overgrowth in the CF mouse small intestine has a role in inflammation and contributes to the failure to thrive in this mouse model of CF.
机译：我们最近报道了囊性纤维化（CF）小鼠小肠的炎症，并且我们认为细菌过度生长是可能的原因。与对照组相比，CF小鼠小肠中细菌16S基因组DNA的定量PCR显示增加了40倍以上。 16S PCR产物的测序和革兰氏染色表明，CF小鼠肠中的大多数细菌为革兰氏阴性。观察到细菌使具有CF的小鼠的肠腔中积累的粘液定居。通过观察CF小鼠肠道隐窝粘液塞中部分分散的Paneth颗粒，提示Paneth细胞防御能力受损，并且该粘液对Paneth细胞杀菌产品具有强烈的免疫反应性。通过用口服抗生素（环丙沙星和甲硝唑）治疗小鼠3周，测试了细菌过度生长在CF肠道炎症中的作用，这使CF小鼠小肠的细菌负荷降低了400倍以上。抗生素治疗降低了炎症相关基因肥大细胞蛋白酶2，富含亮氨酸的α2糖蛋白/富含亮氨酸的高内皮微糖蛋白，细胞因子信号转导抑制因子3，造血细胞转录本1和抵抗素样分子β/的表达。炎症区2，它们不再以与对照水平显着不同的水平表达。肠道细菌的减少也显着改善了CF小鼠的生长，但对野生型小鼠的生长没有影响。这些数据表明，CF小鼠小肠中的细菌过度生长在炎症中起作用，并导致在此CF小鼠模型中无法壮成长。

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