Study on sugar modified antigens and intracellular bacterial pathogens.

伤寒沙门氏菌被称为细胞内病原体，因为它在巨噬细胞内存活。细菌表面覆盖着Vi多糖，n -乙酰半乳糖胺-醛酸均聚物。抗原的表达受渗透压和其他环境因素的控制。当有机体从肠上皮侵入时。伤寒沙门氏菌抑制表面Vi抗原，产生鞭毛蛋白和分泌蛋白，这些因素促进细菌从佩耶氏斑M细胞表面侵入。免疫球蛋白抑制伤寒沙门氏菌与人血型抗原的凝集。斑疹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表达增强，Vi缺失突变体不能在血清中存活，很快被补体杀死。Vi在巨噬细胞内表达最多，Vi缺失突变体在进入巨噬细胞时刺激巨噬细胞，并被巨噬细胞快速加工，这意味着伤寒沙门氏菌需要掩盖表面抗原才能进入巨噬细胞，因为Vi缺失了S，伤寒迅速刺激了巨噬细胞。LPS无应答的巨噬细胞细胞系在Vi缺失巨噬细胞进入时不能被激活。这表明脂多糖受体的识别在识别细菌进入和摄入细菌的加工过程中起主要作用。

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.