Zähringer Ulrich, Lindner Buko, Knirel Yuriy A, van den Akker Willem M R, Hiestand Rosemarie, Heine Holger, Dehio Christoph
Research Center Borstel, Leibniz-Center for Medicine and Biosciences, 23845 Borstel, Germany.
J Biol Chem. 2004 May 14;279(20):21046-54. doi: 10.1074/jbc.M313370200. Epub 2004 Feb 7.
The facultative intracellular pathogen Bartonella henselae is responsible for a broad range of clinical manifestations, including the formation of vascular tumors as a result of increased proliferation and survival of colonized endothelial cells. This remarkable interaction with endotoxin-sensitive endothelial cells and the apparent lack of septic shock are considered to be due to a reduced endotoxic activity of the B. henselae lipopolysaccharide. Here, we show that B. henselae ATCC 49882(T) produces a deep-rough-type lipopolysaccharide devoid of O-chain and report on its complete structure and Toll-like receptor-dependent biological activity. The major short-chain lipopolysaccharide was studied by chemical analyses, electrospray ionization, and matrix-assisted laser desorption/ionization mass spectrometry, as well as by NMR spectroscopy after alkaline deacylation. The carbohydrate portion of the lipopolysaccharide consists of a branched trisaccharide containing a glucose residue attached to position 5 of an alpha-(2-->4)-linked 3-deoxy-d-manno-oct-2-ulosonic acid disaccharide. Lipid A is a pentaacylated beta-(1'-->6)-linked 2,3-diamino-2,3-dideoxy-glucose disaccharide 1,4'-bisphosphate with two amide-linked residues each of 3-hydroxydodecanoic and 3-hydroxyhexadecanoic acids and one residue of either 25-hydroxyhexacosanoic or 27-hydroxyoctacosanoic acid that is O-linked to the acyl group at position 2'. The lipopolysaccharide studied activated Toll-like receptor 4 signaling only to a low extent (1,000-10,000-fold lower compared with that of Salmonella enterica sv. Friedenau) and did not activate Toll-like receptor 2. Some unusual structural features of the B. henselae lipopolysaccharide, including the presence of a long-chain fatty acid, which are shared by the lipopolysaccharides of other bacteria causing chronic intracellular infections (e.g. Legionella and Chlamydia), may provide the molecular basis for low endotoxic potency.
兼性胞内病原体汉赛巴尔通体可引发多种临床表现,包括因被感染的内皮细胞增殖和存活增加而形成血管肿瘤。这种与内毒素敏感内皮细胞的显著相互作用以及明显缺乏脓毒性休克现象,被认为是由于汉赛巴尔通体脂多糖的内毒素活性降低所致。在此,我们表明汉赛巴尔通体ATCC 49882(T)产生一种不含O链的深粗糙型脂多糖,并报道了其完整结构和Toll样受体依赖性生物活性。通过化学分析、电喷雾电离、基质辅助激光解吸/电离质谱以及碱性脱酰化后的核磁共振光谱对主要的短链脂多糖进行了研究。脂多糖的碳水化合物部分由一种分支三糖组成,该三糖含有一个连接在α-(2→4)连接的3-脱氧-D-甘露糖-2-辛酮糖二酸二糖5位上的葡萄糖残基。脂质A是一种五酰化的β-(1'→6)连接的2,3-二氨基-2,3-二脱氧葡萄糖二糖1,4'-双磷酸酯,带有两个酰胺连接的残基,分别为3-羟基十二烷酸和3-羟基十六烷酸,以及一个25-羟基二十六烷酸或27-羟基二十八烷酸残基,该残基通过O连接到2'位的酰基上。所研究的脂多糖仅在低程度上激活Toll样受体4信号传导(与肠炎沙门氏菌弗里登瑙血清型相比低1000 - 10000倍),并且不激活Toll样受体2。汉赛巴尔通体脂多糖的一些不寻常结构特征,包括存在长链脂肪酸,这些特征在其他引起慢性胞内感染的细菌(如嗜肺军团菌和衣原体)的脂多糖中也有,可能为低内毒素效力提供分子基础。