Escherichia coli (E. coli) infection is very common among young growing animals, and zinc supplementation is often used to alleviate inflammation induced by this disease. Therefore, the objective of this study was to evaluate whether chitosan-chelated zinc (CS-Zn) supplementation could attenuate gut injury induced by E. coli challenge and to explore how CS-Zn modulates cecal microbiota and alleviates intestinal inflammation in weaned rats challenged with E. coli. 36 weaned rats (55.65 ± 2.18 g of BW, n = 12) were divided into three treatment groups consisting of unchallenged rats fed a basal diet (Control) and two groups of rats challenged with E. coli and fed a basal diet or a diet containing 640 mg/kg CS-Zn (E. coli + CS-Zn, containing 50 mg/kg Zn) for a 14-day experiment. On days 10 to 12, each rat was given 4 ml of E. coli solution with a total bacteria count of 10¹⁰ CFU by oral gavage daily or normal saline of equal dosage. CS-Zn supplementation mitigated intestinal morphology impairment (e.g. higher crypt depth and lower macroscopic damage index) induced by E. coli challenge (P < 0.05), and alleviated the increase of Myeloperoxidase (MPO) activity after E. coli challenge (P < 0.05). 16S rRNA sequencing analyses revealed that E. coli challenge significantly increased the abundance of Verrucomicrobia and E. coli (P < 0.05). However, CS-Zn supplementation increased the abundance of Lactobacillus and decreased the relative abundance of Proteobacteria, Desulfovibrio and E. coli (P < 0.05). The concentrations of butyrate in the cecal digesta, which decreased due to the challenge, were higher in the E. coli + CS-Zn group (P < 0.05). In addition, CS-Zn supplementation significantly prevented the elevation of pro-inflammatory cytokines IL-6 concentration and up-regulated the level of anti-inflammatory cytokines IL-10 in cecal mucosa induced by E. coli infection (P < 0.05). In conclusion, these results indicate that CS-Zn produces beneficial effects in alleviating gut mucosal injury of E. coli challenged rats by enhancing the intestinal morphology and modulating cecal bacterial composition, as well as attenuating inflammatory response.

中文翻译：

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脱乙酰壳多糖螯合的锌可调节盲肠微生物，并减弱受到大肠杆菌攻击的断奶大鼠的炎症反应。

大肠杆菌（E. coli）感染在年轻的成长动物中非常常见，并且补充锌常用于缓解由该疾病引起的炎症。因此，本研究的目的是评估壳聚糖螯合锌（CS-Zn）的添加是否能减轻大肠杆菌激发所致的肠道损伤，并探讨CS-Zn如何调节盲肠微生物对盲肠菌群和肠道炎症的影响。大肠杆菌。将36只断奶的大鼠（55.65±2.18 g BW，n = 12）分为三个治疗组，分别为无挑战的大鼠喂食基础饮食（对照组）和两组被大肠杆菌攻击并喂食基础饮食或饮食的大鼠含有640 mg / kg CS-Zn（E.大肠杆菌+ CS-Zn，含50 mg / kg锌）进行14天实验。在第10至12天，通过每天口服管饲或相同剂量的生理盐水，给每只大鼠4ml的大肠杆菌溶液，其细菌总数为10 ¹⁰ CFU。CS-Zn补充剂减轻了大肠杆菌激发引起的肠道形态损害（例如，隐窝深度增加和宏观损害指数降低）（P <0.05），并减轻了大肠杆菌激发后髓过氧化物酶（MPO）活性的增加（P <0.05） ）。16S rRNA测序分析表明，大肠杆菌挑战显着增加了疣状微生物和大肠杆菌的丰度（P<0.05）。然而，CS-Zn的添加增加了乳酸杆菌的丰度，降低了变形杆菌，脱硫弧菌和大肠杆菌的相对丰度（P <0.05）。大肠杆菌+ CS-Zn组的盲肠消化物中丁酸盐的浓度由于挑战而降低，但较高（P <0.05）。此外，CS-Zn的添加显着阻止了大肠杆菌感染引起的盲肠粘膜中促炎细胞因子IL-6浓度的升高，并上调了抗炎细胞因子IL-10的水平（P<0.05）。总之，这些结果表明，CS-Zn通过增强肠道形态和调节盲肠细菌组成以及减弱炎症反应，在缓解大肠杆菌攻击的大鼠的肠道粘膜损伤方面产生有益的作用。