Withanage G S K, Kaiser Pete, Wigley Paul, Powers Claire, Mastroeni Pietro, Brooks Heather, Barrow Paul, Smith Adrian, Maskell Duncan, McConnell Ian
Centre for Veterinary Science, Department of Clinical Veterinary Medicine, University of Cambridge, Cambridge CB3 0ES, United Kingdom.
Infect Immun. 2004 Apr;72(4):2152-9. doi: 10.1128/IAI.72.4.2152-2159.2004.
Poultry meat and eggs contaminated with Salmonella enterica serovar Enteritidis or Salmonella enterica serovar Typhimurium are common sources of acute gastroenteritis in humans. However, the exact nature of the immune mechanisms protective against Salmonella infection in chickens has not been characterized at the molecular level. In the present study, bacterial colonization, development of pathological lesions, and proinflammatory cytokine and chemokine gene expression were investigated in the liver, spleen, jejunum, ileum, and cecal tonsils in newly hatched chickens 6, 12, 24, and 48 h after oral infection with Salmonella serovar Typhimurium. Very high bacterial counts were found in the ileum and cecal contents throughout the experiment, whereas Salmonella started to appear in the liver only from 24 h postinfection. Large numbers of heterophils, equivalent to neutrophils in mammals, and inflammatory edema could be seen in the lamina propria of the intestinal villi and in the liver. Interleukin 8 (IL-8), K60 (a CXC chemokine), macrophage inflammatory protein 1 beta, and IL-1 beta levels were significantly upregulated in the intestinal tissues and in the livers of the infected birds. However, the spleens of the infected birds show little or no change in the expression levels of these cytokines and chemokines. Increased expression of the proinflammatory cytokines and chemokines (up to several hundred-fold) correlated with the presence of inflammatory signs in those tissues. This is the first description of in vivo expression of chemokines and proinflammatory cytokines in response to oral infection with Salmonella in newly hatched chickens.
被肠炎沙门氏菌或鼠伤寒沙门氏菌污染的禽肉和禽蛋是人类急性肠胃炎的常见来源。然而,鸡体内抵御沙门氏菌感染的免疫机制的确切性质在分子水平上尚未得到明确。在本研究中,对刚孵化出的雏鸡口服感染鼠伤寒沙门氏菌后6、12、24和48小时,对其肝脏、脾脏、空肠、回肠和盲肠扁桃体中的细菌定植、病理损伤发展以及促炎细胞因子和趋化因子基因表达进行了研究。在整个实验过程中,回肠和盲肠内容物中发现了非常高的细菌数量,而沙门氏菌直到感染后24小时才开始出现在肝脏中。在肠绒毛固有层和肝脏中可见大量相当于哺乳动物中性粒细胞的异嗜性粒细胞和炎性水肿。感染鸡的肠道组织和肝脏中白细胞介素8(IL-8)、K60(一种CXC趋化因子)、巨噬细胞炎性蛋白1β和IL-1β水平显著上调。然而,感染鸡的脾脏中这些细胞因子和趋化因子的表达水平几乎没有变化或没有变化。促炎细胞因子和趋化因子表达的增加(高达数百倍)与这些组织中炎症迹象的存在相关。这是首次描述雏鸡口服感染沙门氏菌后趋化因子和促炎细胞因子在体内的表达情况。