Southern Plains Agricultural Research Center, Agricultural Research Service, U.S. Department of Agriculture, College Station, Texas 77845, USA.
Foodborne Pathog Dis. 2012 Dec;9(12):1104-10. doi: 10.1089/fpd.2012.1233. Epub 2012 Oct 15.
Poultry is a major reservoir for foodborne Salmonella serovars. Salmonella Typhimurium, Salmonella Enteritidis, Salmonella Heidelberg, Salmonella Kentucky, and Salmonella Senftenberg are the most prevalent serovars in U.S. poultry. Information concerning the interactions between different Salmonella species and host cells in poultry is lacking. In the present study, the above mentioned Salmonella serovars were examined for invasion, intracellular survival, and their ability to modulate oxidative burst and nitric oxide (NO) responses in chicken macrophage HD11 cells. All Salmonella serovars demonstrated similar capacity to invade HD11 cells. At 24 h post-infection, a 36-43% reduction of intracellular bacteria, in log(10)(CFU), was observed for Salmonella Typhimurium, Salmonella Heidelberg, Salmonella Kentucky, and Salmonella Senftenberg, whereas a significantly lower reduction (16%) was observed for Salmonella Enteritidis, indicating its higher resistance to the killing by HD11 cells. Production of NO was completely diminished in HD11 cells infected with Salmonella Typhimurium and Salmonella Enteritidis, but remained intact when infected with Salmonella Heidelberg, Salmonella Kentucky, and Salmonella Senftenberg. Phorbol myristate acetate-stimulated oxidative burst in HD11 cells was greatly impaired after infection by each of the five serovars. When newly hatched chickens were challenged orally, a high rate (86-98%) of systemic infection (Salmonella positive in liver/spleen) was observed in birds challenged with Salmonella Typhimurium, Salmonella Enteritidis, Salmonella Heidelberg, and Salmonella Kentucky, while only 14% of the birds were Salmonella Senftenberg positive. However, there was no direct correlation between systemic infection and in vitro differential intracellular survival and modulation of NO response among the tested serovars.
家禽是食源性沙门氏菌血清型的主要宿主。在美国的家禽中,最常见的沙门氏菌血清型包括鼠伤寒沙门氏菌、肠炎沙门氏菌、海德堡沙门氏菌、肯塔基沙门氏菌和森夫滕贝格沙门氏菌。关于不同沙门氏菌血清型与家禽宿主细胞之间相互作用的信息尚不清楚。在本研究中,研究了上述沙门氏菌血清型在鸡巨噬细胞 HD11 细胞中的侵袭、细胞内存活能力,以及它们对氧化爆发和一氧化氮(NO)反应的调节能力。所有沙门氏菌血清型均显示出类似的侵袭 HD11 细胞的能力。在感染后 24 小时,鼠伤寒沙门氏菌、海德堡沙门氏菌、肯塔基沙门氏菌和森夫滕贝格沙门氏菌的细胞内细菌数量减少了 36-43%(log10(CFU)),而肠炎沙门氏菌的减少幅度明显较低(16%),表明其对 HD11 细胞杀伤的抵抗力更高。感染鼠伤寒沙门氏菌和肠炎沙门氏菌的 HD11 细胞中 NO 的产生完全被抑制,但感染海德堡沙门氏菌、肯塔基沙门氏菌和森夫滕贝格沙门氏菌时则保持完整。五种血清型感染后,HD11 细胞中佛波醇肉豆蔻酸酯刺激的氧化爆发大大受损。当刚孵出的小鸡经口攻毒时,用鼠伤寒沙门氏菌、肠炎沙门氏菌、海德堡沙门氏菌和肯塔基沙门氏菌攻毒的鸡中有 86-98%(肝脏/脾脏中沙门氏菌阳性)发生全身性感染,而用森夫滕贝格沙门氏菌攻毒的鸡中只有 14%沙门氏菌阳性。然而,在测试的血清型中,系统感染率(肝脏/脾脏中沙门氏菌阳性)与细胞内生存差异和 NO 反应调节的体外差异之间没有直接相关性。