Study on sugar modified antigens and intracellular bacterial pathogens.

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存活。细菌的表面覆盖有Vi多糖，N-乙酰基半乳糖胺-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。色葡萄伤寒杆菌抑制表面Vi抗原，产生鞭毛蛋白和分泌蛋白，这些因子促进细菌从派尔集合淋巴结M细胞表面侵入。Vi压制了S。伤寒杆菌与人血型抗原凝集。S.伤寒沙门氏菌是引起这种凝集的主要原因，这种凝集可能促进细菌进入上皮细胞，Vi在血液和巨噬细胞中表达增强，Vi缺失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高，Vi缺失突变体在进入巨噬细胞的过程中刺激巨噬细胞，并迅速被巨噬细胞加工。伤寒杆菌需要掩蔽表面抗原才能进入巨噬细胞，因为Vi缺失了伤寒杆菌，伤寒杆菌迅速刺激巨噬细胞。LPS非应答性巨噬细胞系在Vi缺失的巨噬细胞进入时不能被激活。这表明LPS受体的识别在识别细菌进入和消化细菌的加工中起主要作用。

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.