Weening Eric H, Barker Jared D, Laarakker Marijke C, Humphries Andrea D, Tsolis Renée M, Bäumler Andreas J
Department of Medical Microbiology and Immunology, School of Medicine, University of California at Davis, One Shields Ave., Davis, CA 95616-8645, USA.
Infect Immun. 2005 Jun;73(6):3358-66. doi: 10.1128/IAI.73.6.3358-3366.2005.
Salmonella enterica serotype Typhimurium causes human infections that can frequently be traced back through the food chain to healthy livestock whose intestine is colonized by the pathogen. Little is known about the genes important for intestinal carriage of S. enterica serotype Typhimurium in vertebrate animals. Here we characterized the role of 10 fimbrial operons, agf, fim, lpf, pef, bcf, stb, stc, std, stf, and sth, using competitive infection experiments performed in genetically susceptible (BALB/c) and resistant (CBA) mice. Deletion of agfAB, fimAICDHF, lpfABCDE, pefABCDI, bcfABCDEFG, stbABCD, stcABCD, stdAB, stfACDEFG, or sthABCDE did not reduce the ability of S. enterica serotype Typhimurium to colonize the spleen and cecum of BALB/c mice 5 days after infection. Similarly, deletion of agfAB, fimAICDHF, pefABCDI, and stfACDEFG did not result in reduced recovery of S. enterica serotype Typhimurium from fecal samples collected from infected CBA mice over a 30-day time period. However, S. enterica serotype Typhimurium strains carrying deletions in lpfABCDE, bcfABCDEFG, stbABCD, stcABCD, stdAB, or sthABCDE were recovered at significantly reduced numbers from the feces of CBA mice. There was a good correlation (R(2) = 0.9626) between competitive indices in the cecum and fecal samples of CBA mice at 30 days after infection, suggesting that the recovery of S. enterica serotype Typhimurium from fecal samples closely reflected its ability to colonize the cecum. Collectively, these data show that six fimbrial operons (lpf, bcf, stb, stc, std, and sth) contribute to long-term intestinal carriage of S. enterica serotype Typhimurium in genetically resistant mice.
肠炎沙门氏菌鼠伤寒血清型可引发人类感染，这类感染常常能通过食物链追溯到健康家畜，其肠道已被该病原体定殖。关于肠炎沙门氏菌鼠伤寒血清型在脊椎动物肠道定殖中起重要作用的基因，人们了解甚少。在此，我们利用在基因易感（BALB/c）和抗性（CBA）小鼠中进行的竞争性感染实验，对10个菌毛操纵子（agf、fim、lpf、pef、bcf、stb、stc、std、stf和sth）的作用进行了表征。缺失agfAB、fimAICDHF、lpfABCDE、pefABCDI、bcfABCDEFG、stbABCD、stcABCD、stdAB、stfACDEFG或sthABCDE，并不会降低肠炎沙门氏菌鼠伤寒血清型在感染后5天定殖于BALB/c小鼠脾脏和盲肠的能力。同样，缺失agfAB、fimAICDHF、pefABCDI和stfACDEFG，并不会导致在30天的时间段内从感染的CBA小鼠采集的粪便样本中回收的肠炎沙门氏菌鼠伤寒血清型数量减少。然而，携带lpfABCDE、bcfABCDEFG、stbABCD、stcABCD、stdAB或sthABCDE缺失的肠炎沙门氏菌鼠伤寒血清型菌株，从CBA小鼠粪便中回收的数量显著减少。感染后30天，CBA小鼠盲肠和粪便样本中的竞争指数之间存在良好的相关性（R(2) = 0.9626），这表明从粪便样本中回收肠炎沙门氏菌鼠伤寒血清型密切反映了其定殖于盲肠的能力。总体而言，这些数据表明，6个菌毛操纵子（lpf、bcf、stb、stc、std和sth）有助于肠炎沙门氏菌鼠伤寒血清型在基因抗性小鼠中长期定殖于肠道。
