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92 Postnatal growth retardation impairs intestinal mucosal barrier in piglets

机译:92产后迟缓仔猪危害肠粘膜屏障

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摘要

The piglets with postnatal growth retardation (PGR) have high mortality and morbidity during their growth and development. Abnormal development of small intestine is casually implicated in impaired growth, but the exact mechanism still remains poorly understood. Thus, the present study investigated the immune profiles related to intestinal mucosal barrier in PGR and healthy piglets. The plasma sample, middle segments of small intestine, and the intestinal mucosa were obtained from healthy and PGR piglets at 42d of age. Compared to healthy piglets, higher plasma concentrations of diamine oxidase and D-lactate were observed in PGR piglets (P < 0.05). Decreased villous height, ratio of villous height to crypt depth, as well as sparse villi, jagged microvilli were also found in jejunum and ileum of PGR piglets. PGR also decreased the percentage of proliferating cell nuclear antigen (PCNA)-positive cells, as well as abundance of Zonula occludens-1, Occludin, Claudin-1, and E-cadherin mRNA and protein in jejunal and ileal mucosa (P < 0.05). The lower concentration of sIgA in jejunal mucosa, and lysozyme in both jejunal and ileal mucosa, but higher level of β-defensins in the ileal mucosa were observed in PGR piglets as compared to healthy piglets (P < 0.05). The percentage of CD68-positive cells were significantly increased, but the levels of P-glycoprotein were decreased in jejunum and ileum from PGR piglets (P < 0.01). Moreover, the expression of proteins involved in p38 MAPK/NF-kB pathway was significantly upregulated in jejunal and ileal mucosa from PGR piglets (P < 0.05). Collectively, these results indicated that the PGR piglets exhibited impaired intestinal integrity, and decreased capacity of mucosal immune function, which may result in severe inflammatory response via the activation of p38 MAPK/NF-kB pathway. Our findings may have important implications in the prevention and treatment of the intestinal mucosal barrier dysfunction in piglets.
机译:具有产后生长迟缓(PGR)的仔猪在其生长和发育过程中具有高死亡率和发病率。小肠的异常发育随着增长的损害而平时涉及,但确切的机制仍然仍然清晰。因此,本研究研究了PGR和健康仔猪中与肠粘膜屏障有关的免疫谱。等离子体样品,小肠的中间段,和肠粘膜在42d时代的健康和PGR仔猪获得。与健康仔猪相比,在PGR仔猪中观察到较高的二胺氧化酶和D-乳酸的血浆浓度(P <0.05)。绒毛高度下降,绒毛高度与隐窝深度的比例,以及稀疏绒毛,锯齿状的微血管也被发现在JEJUNUM和PGR仔猪的回肠。 PGR还降低了延长细胞核抗原(PCNA)阳性细胞的百分比,以及JEUNAL和ILEAL MUCOSA中的Zonula occludens-1,occludin,Claudin-1和E-Cadherin mRNA和蛋白质(P <0.05) 。与健康仔猪相比,Jejunal粘膜中的粘液粘膜中SIGA的浓度较低,含有髂骨和髂骨粘膜,但在PGR仔猪中观察到髂骨粘膜中的β-脱蜡素较高(P <0.05)。 CD68阳性细胞的百分比显着增加,但是PGR仔猪的Jejunum和Hileum中,p-糖蛋白的水平降低(P <0.01)。此外,在PGR仔猪的JEJUNAL和ILEAL粘膜中显着上调了参与P38 MAPK / NF-KB途径的蛋白质的表达(P <0.05)。总的来说,这些结果表明,PGR仔猪表现出患有受损的肠完整性,并且降低了粘膜免疫功能的能力,这可能导致P38 Mapk / NF-KB途径的激活产生严重的炎症反应。我们的研究结果可能对预防和治疗仔猪肠粘膜屏障功能障碍的重要意义。

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