Popoff M Y
Institut Pasteur, Unité des Entérobactéries, Unité INSERM 199, Paris.
Bull Acad Natl Med. 1991 Jun-Jul;175(6):811-21.
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)
鼠伤寒沙门氏菌是一种兼性胞内病原体,可在自然感染或实验感染的小鼠中引起全身感染。经口感染后,鼠伤寒沙门氏菌定殖于回肠黏膜和派尔集合淋巴结,并侵入引流的肠系膜淋巴结。从这些主要感染部位,细菌扩散到网状内皮系统,并在脾脏和肝脏中迅速增殖。几个毒力因子由染色体基因编码。鼠伤寒沙门氏菌黏附并侵入上皮细胞的能力与鞭毛、I型菌毛和甘露糖抗性血凝活性有关。通过比较同基因菌株的毒力,发现这些特性起的作用较小,并非完全毒力表达所必需。现在很清楚,其他表面结构对鼠伤寒沙门氏菌的侵袭能力很重要。为了在网状内皮系统中繁殖,完整的脂多糖对于细菌抵抗血清杀菌活性和造成组织损伤是必需的。沙门氏菌进化出一种特殊的铁结合配体,称为肠杆菌素,以获取其繁殖所需的铁。肠杆菌素与宿主铁结合蛋白(转铁蛋白或乳铁蛋白)竞争,以确保细菌所需的铁。尽管沙门氏菌中存在肠毒素仍存在争议,但现在有大量证据支持这一概念。最近,一个编码肠毒素的基因已从鼠伤寒沙门氏菌中克隆出来,并在大肠杆菌中表达。鼠伤寒沙门氏菌菌株含有一个90千碱基(kb)的质粒,这对毒力至关重要。该质粒编码沙门氏菌在肝脏和脾脏中复制所需的毒力因子。据推测,该质粒使鼠伤寒沙门氏菌能够在库普弗细胞和脾巨噬细胞中繁殖。质粒的毒力相关区域使无质粒菌株恢复了完全毒力。转座子插入诱变证明存在两个DNA序列,命名为Vir A和Vir B,它们对毒力表达至关重要。Vir A区域已测序;它编码四种表观分子量分别为27000、28000、33000和70000的多肽。Vir B区域编码两种分子量分别为38000和43000的多肽。为了鉴定有助于伤寒沙门氏菌侵袭HeLa细胞的细菌成分,我们克隆了一段30 kb的DNA序列,这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表型。从这个DNA片段中,亚克隆了一段487 bp的短片段,进行了测序,并用作探针来检测沙门氏菌。(摘要截断于400字)