Tang Ying, Jones Michael, Barrow Paul A, Foster Neil
School of Veterinary Medicine and Science, University of Nottingham, Nottingham LE12 5RD, UK.
SRUC Aberdeen Campus, Craibstone Estate, Ferguson Building, Aberdeen AB21 9YA, UK.
Pathogens. 2020 Oct 15;9(10):843. doi: 10.3390/pathogens9100843.
serovar Gallinarum (. Gallinarum) is the cause of typhoid in chickens but the immune factors that may facilitate the development of typhoid have not been fully elucidated. We show that, in contrast to non-typhoid . Enteritidis infection, . Gallinarum significantly reduced nitrite ion production and expression of mRNA for heterophil granulocyte chemoattractants CXCLi2 and IL-6 in chicken monocyte-derived macrophages (chMDMs) ( < 0.05) at 6 h post-infection (pi). . Gallinarum also reduced IFN-γ and IL-17 expression by CD4 lymphocytes cultured with infected chMDMs for 5 days but did not induce a Th2 phenotype or anergy. In vivo, . Gallinarum also induced significantly lower expression of CXCLi1, CXCLi2, IL-1β, IL-6 and iNOS mRNA in the caecal tonsil by day 2 pi ( < 0.05-0.01) and consistently lower levels of IFN-γ, IL-18, IL-12, and IL-17. In the spleen, . Gallinarum induced significantly lower levels of iNOS and IFN-γ ( < 0.01 and 0.05 respectively) and consistently lower levels of IL-18 and IL-12 but significantly greater ( < 0.01) expression of anti-inflammatory IL-10 at day 4 and 5 pi when compared to . Enteritidis. This immune phenotype was associated with transit from the intestinal tissues to the liver by . Gallinarum, not observed following . Enteritidis infection. In conclusion, we report an immune mechanism that may facilitate typhoid disease in . Gallinarum-infected chickens. However, down-regulation of inflammatory mediators, upregulation of IL-10, and associated liver colonisation are also characteristic of human typhoid, suggesting that this may also be a useful model of typhoid in humans.
鸡伤寒沙门氏菌（鸡沙门氏菌）是鸡伤寒的病原体，但促进鸡伤寒发展的免疫因素尚未完全阐明。我们发现，与非伤寒肠炎沙门氏菌感染相比，鸡沙门氏菌在感染后6小时（pi）显著降低了鸡单核细胞衍生巨噬细胞（chMDMs）中亚硝酸根离子的产生以及嗜异性粒细胞趋化因子CXCLi2和IL-6的mRNA表达（P<0.05）。鸡沙门氏菌还降低了与感染的chMDMs共培养5天的CD4淋巴细胞中IFN-γ和IL-17的表达，但未诱导Th2表型或无反应性。在体内，到感染后第2天，鸡沙门氏菌还显著降低了盲肠扁桃体中CXCLi1、CXCLi2、IL-1β、IL-6和iNOS mRNA的表达（P<0.05 - 0.01），并持续降低IFN-γ、IL-18、IL-12和IL-17的水平。在脾脏中，与肠炎沙门氏菌相比，鸡沙门氏菌在感染后第4天和第5天显著降低了iNOS和IFN-γ的水平（分别为P<0.01和P<0.05），并持续降低IL-18和IL-12的水平，但抗炎性IL-10的表达显著更高（P<0.01）。这种免疫表型与鸡沙门氏菌从肠道组织转移至肝脏有关，而肠炎沙门氏菌感染后未观察到这种情况。总之，我们报道了一种可能促进鸡沙门氏菌感染鸡发生鸡伤寒疾病的免疫机制。然而，炎症介质的下调、IL-10的上调以及相关的肝脏定植也是人类伤寒的特征，这表明这也可能是人类伤寒的一个有用模型。
