鸭源新城疫强毒株对番鸭细胞因子及Toll样受体mRNA表达的影响

为研究人工感染鸭源新城疫强毒株(Md/CH/LGD/1/2005)诱导番鸭细胞因子及Toll样受体基因的表达情况,选用80只15日龄SPF番鸭,随机分为攻毒组和对照组,每组各40只,攻毒组以滴鼻点眼的方式接种1×107.0EID50鸭源基因Ⅶ型新城疫病毒(NDV)Md/CH/LGD/1/2005,对照组接种灭菌的磷酸盐...

Duck mRNA expression of cytokines and toll receptors induced by duck-origin virulent Newcastle disease virus

This experiment was conducted to study the expression of the duck cytokines and toll-like receptor(TLR)genes of duck artificially infected with duck-origin Newcastle disease virus(NDV)Md/CH/LGD/1/2005 strain.Eighty 15-day-old SPF Muscovy ducks were randomly divided into the infected group and the control group,each group 40.The infected group was intraocularly inoculated with 1×107.0 EID50 duck-origin genotypeⅦNDV strain(Md/CH/LGD/1/2005),and the control group was mock-inoculated with phosphate-buffered saline(PBS).Ten ducks in each group were dissected and killed at 36 hour post infection(hpi),72 hpi,7 day post infection(dpi)and 25 dpi,respectively.Bone marrow,spleen,cecal tonsil,Hadard’s gland and Bursa samples of each duck were collected.Real-time RT-PCR was used to detect NDV load,expression of cytokines and toll-like receptor genes in tissues.The results showed that the viral load in all tissues reached the highest at 72 hpi except Hadard’s gland.However,no viral load was detected in all tissues of the control group.Compared with the control group,IL-1βexpression was significantly increased in bursa(36 hpi)and Harder’s gland(7 dpi)(P<0.05).In addition,m RNA expression of IL-2,IL-6,IL-18 and IL-20 were significantly increased in the spleen on 7 dpi(P<0.05).TLR3,TLR15 and TLR21 were highly expressed in the bursa of Fabricius(P<0.05),with the same expression trend,the response to NDV infection have a synergistic effect.Expression of TLR5 was increased significantly in bone marrow,spleen,cecal tonsil and bursa(P<0.05).TLR7 expression was upregulated in bone marrow and bursa of Fabricius on 7 dpi(P<0.05).In summary,immune responses of duck against NDV infection may be through TLR-dependent signal pathway,then regulated the host antiviral response.