Salmonella serotype Typhimurium is a facultative intracellular pathogen that causes a systemic infection in naturally, or experimentally, infected mice. After oral contamination, Typhimurium colonizes the ileal mucosa and Peyer's patches and invades draining mesenteric lymph nodes. From these primary sites of infection, bacteria dissiminate to the reticuloendothelial system and proliferate rapidly in spleen and liver. Several virulence factors are encoded by chromosomal genes. The ability of Typhimurium to adhere to and invade epithelial cells has been associated with flagella, pili of type I and mannose-resistant haemagglutinating activity. By comparing the virulence of isogenic strains, it appeared that these traits played a marginal role and were not essential for full virulence expression. It is now clear that other surface structures are important for the invasiness capacity of Typhimurium. To multiply in the reticuloendothelial system, a complete lipopolysaccharide is necessary for the bacteria in resisting serum bactericidal activity and producing tissue damage. Salmonella have evolved a specialized iron-binding ligand, termed enterobactin, to acquire iron necessary for their multiplication. Enterobactin competes with the host iron-binding proteins (transferrin or lactoferrin) to secure the iron required by the bacteria. Though the presence of an enterotoxin in Salmonella is still controversial, there is now substantial evidence to support this concept. Recently, a gene encoding an enterotoxin has been cloned from Typhimurium and expressed in E. coli. Typhimurium strains harbour a 90 kilobases (kb) plasmid which is essential for virulence. This plasmid encodes virulence factors required for replication of Salmonella in liver and spleen. It was postulated that the plasmid allowed Typhimurium to multiply in Kupffer cells and in splenic macrophages. The virulence-associated region of the plasmid restored full virulence to plasmidless strains. Transposon insertion mutagenesis demonstrated the existence of two DNA sequences, designated Vir A and Vir B, which are essential for virulence expression. The Vir A region has been sequenced; it encodes four polypeptides with apparent molecular mass of 27,000, 28,000, 33,000 and 70,000. The Vir B region encodes two polypeptides of 38,000 and 43,000. In an attempt to identify bacterial components contributing to invasion of HeLa cells by Salmonella serovar Typhi, we cloned a 30 kb DNA sequence necessary for entry of bacteria into epithelial cells. However, this sequence is not sufficient for conferring an invasive phenotype to E. coli strains. From this DNA fragment, a short segment of 487 bp was subcloned, sequenced and used as probe to detect Salmonella.(ABSTRACT TRUNCATED AT 400 WORDS)

译文

沙门氏菌血清型鼠伤寒沙门氏菌是一种兼性的细胞内病原体,可在自然或实验感染的小鼠中引起全身性感染。口腔污染后,鼠伤寒菌定居在回肠粘膜和派伊尔斑片上,并侵入排泄的肠系膜淋巴结。细菌从这些主要的感染部位扩散到网状内皮系统,并在脾脏和肝脏中迅速繁殖。几种毒力因子由染色体基因编码。鼠伤寒杆菌粘附和侵袭上皮细胞的能力与鞭毛,I型菌毛和抗甘露糖的血凝活性有关。通过比较同基因菌株的毒力,看来这些性状只发挥了边际作用,对于完整的毒力表达并不是必不可少的。现在清楚的是,其他表面结构对于鼠伤寒的侵袭能力也很重要。为了在网状内皮系统中繁殖,细菌必须具有完整的脂多糖才能抵抗血清杀菌活性并产生组织损伤。沙门氏菌已经进化出一种专门的铁结合配体,称为肠杆菌素,以获取繁殖所需的铁。肠杆菌素与宿主铁结合蛋白(运铁蛋白或乳铁蛋白)竞争,以确保细菌所需的铁。尽管沙门氏菌中肠毒素的存在仍存在争议,但现在有大量证据支持这一概念。最近,已经从鼠伤寒中克隆了编码肠毒素的基因并在大肠杆菌中表达。鼠伤寒沙门氏菌菌株带有一个90 kb的质粒,该质粒对于毒力至关重要。该质粒编码沙门氏菌在肝和脾中复制所需的毒力因子。推测该质粒允许鼠伤寒杆菌在库普弗细胞和脾巨噬细胞中繁殖。质粒的毒力相关区域恢复了无质粒菌株的全部毒力。转座子插入诱变表明存在两个DNA序列,命名为Vir A和Vir B,这对于毒力表达至关重要。 Vir A区已被测序;它编码四种表观分子量分别为27,000、28,000、33,000和70,000的多肽。 Vir B区编码两个38,000和43,000的多肽。为了鉴定导致鼠伤寒沙门氏菌侵袭HeLa细胞的细菌成分,我们克隆了一个30 k​​b的DNA序列,该序列是细菌进入上皮细胞所必需的。然而,该序列不足以赋予大肠杆菌菌株侵袭性表型。从该DNA片段中克隆了487 bp的短片段,进行了测序并用作检测沙门氏菌的探针。(摘要截短了400字)

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