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Study on sugar modified antigens and intracellular bacterial pathogens.

糖修饰抗原和胞内细菌病原体的研究。

基本信息

批准号：
10470068
负责人：
EZAKI Takayuki
金额：
$ 2.82万
依托单位：
Gifu University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (B)
财政年份：
1998
资助国家：
日本
起止时间：
1998 至 1999
项目状态：
已结题

项目摘要

Salmonella typhi is known as an intracellular pathogen because the organism survives inside macrophages. The surface of the bacteria is covered with Vi polysaccharide, N-acetyl galactosamine-uronic acid homopolymer. The expression of the antigen is controlled by osmolarity and other environmental factors. When the organism invades from intestinal epithelium. The s. typhi suppresses surface Vi antigen and produces flagellin and secreted proteins, these factors promote the bacterial invasion from the surface of M cells of Peyer's patches. The Vi suppressed S. typhi agglutinate with human blood type antigen. The surface omp C protein of S. typhi was responsible for this agglutination, This agglutination maybe promote bacterial entry into epithelial cells.Vi expression is promoted in blood and inside macrophages, Vi deleted mutants cannot survive in serum and quickly killed by complement. Vi was maximally expressed inside macrophages, Vi deleted mutants stimulated macrophages during the entry into macrophages and quickly processed by macrophages, This means that S. typhi needs to mask surface antigen to enter macrophage because Vi deleted S, typhi quickly stimulated macrophages. LPS nonresponsive macrophages cell line could not activated during the entry of Vi deleted macrophages. This suggests that recognition of LPS receptor play a major role to recognize bacterial entry and processing of ingested bacteria.

伤寒沙门氏菌被称为细胞内病原体，因为该生物体在巨噬细胞内生存。细菌表面覆盖有Vi多糖、N-乙酰半乳糖胺-糖醛酸均聚物。抗原的表达受渗透压和其他环境因素控制。当微生物从肠上皮侵入时。的。伤寒杆菌抑制表面Vi抗原并产生鞭毛蛋白和分泌蛋白，这些因子促进细菌从派伊尔集结M细胞表面侵入。 Vi抑制伤寒沙门氏菌与人血型抗原的凝集。伤寒沙门氏菌的表面omp C蛋白负责这种凝集，这种凝集可能促进细菌进入上皮细胞。Vi在血液和巨噬细胞内的表达得到促进，Vi缺失的突变体不能在血清中存活并很快被补体杀死。 Vi在巨噬细胞内表达最大，Vi缺失突变体在进入巨噬细胞过程中刺激巨噬细胞并快速被巨噬细胞处理，这意味着伤寒沙门氏菌需要掩蔽表面抗原才能进入巨噬细胞，因为Vi缺失S，伤寒沙门氏菌快速刺激巨噬细胞。 LPS无反应性巨噬细胞系在Vi删除的巨噬细胞进入期间不能被激活。这表明LPS受体的识别在识别细菌进入和摄入细菌的处理中发挥着重要作用。