Differential gene expression profiles of β-defensins in the crop, intestine, and spleen using a necrotic enteritis model in 2 commercial broiler chicken lines

Differential gene expression profiles of β-defensins in the crop, intestine, and spleen using a necrotic enteritis model in 2 commercial broiler chicken lines
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DOI:
10.3382/ps.2011-01948
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发表时间:
2012-05-01
期刊:
影响因子:
4.4
通讯作者:
Lillehoj, H. S.
Lillehoj, H. S.
中科院分区:
农林科学2区
文献类型:
--
作者:
Hong, Y. H.;Song, W.;Lillehoj, H. S.

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在坏死性肠炎(NE)疾病模型中,在2个遗传上不同的商业肉鸡品系:Ross和Cobb中评估了禽β-防御素(AvBD)mRNA表达水平的变化。通过先前建立的共感染模型,使用口服巨型艾美耳球虫感染,然后进行产气荚膜梭菌攻毒,在肠道中启动NE。在检查的14种AvBD类型中,存在AvBD转录物的组织特异性表达:AvBD 1,AvBD 7和AvBD 9在作物中; AvBD 8,AvBD 10和AvBD 13;在肠中,AvBD 1和AvBD 7在脾脏中。两个不同的商品肉鸡品系在共感染E. maxima和C.产气荚膜杆菌,其中R系鸡通常显示出比C株更高的表达水平。两种鸡株均显示出促炎细胞因子的基因表达水平增强,如脾中的IL-1 β、IL-6、IL-17 F和TNFSF 15以及肠中的TNFSF 15,而IL-17 F仅在NE感染后的R系鸡的肠中显著增加。虽然防御素和细胞因子之间的相互作用在决定宿主对NE病原体的先天免疫应答的结果方面的确切性质仍有待研究,但肠道、作物和脾脏中β-防御素和促炎细胞因子基因表达水平的差异可以解释2种商品肉鸡品系对NE的易感性和易感性。
Changes in the expression levels of avian beta-defensin (AvBD) mRNA were evaluated in necrotic enteritis (NE) disease model in 2 genetically disparate commercial broiler chicken lines: Ross and Cobb. The NE was initiated in the gut by a previously established co-infection model using oral Eimeria maxima infection followed by a Clostridium perfringens challenge. Among the 14 AvBD types examined, there was a tissue-specific expression of AvBD transcripts: AvBD1, AvBD7, and AvBD9 in the crop; AvBD8, AvBD10, and AvBD13; in the intestine and AvBD1 and AvBD7 in the spleen. The 2 different commercial broiler chicken lines showed differential gene expression patterns of AvBD transcripts following co-infection with E. maxima and C. perfringens, with R-line chickens generally showing higher expression levels than the C strain. Both chicken strains showed enhanced gene expression levels of proinflammatory cytokines, such as IL-1 beta, IL-6, IL-17F, and TNFSF15 in spleen, and TNFSF15 in intestine, whereas IL-17F was significantly increased only in the intestine of R-line chickens following NE infection. Although the exact nature of interactions between defensins and cytokines in determining the outcome of host innate immune responses to the pathogens of NE remains to be investigated, the differences in gene expression levels of beta-defensins and proinflammatory cytokines in the intestine, crop, and spleen could explain the predisposed disease resistance and susceptibility to NE in the 2 commercial broiler chicken lines.