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用F4 + 大肠杆菌对小鼠和仔猪进行肠胃外接种,可抑制口服感染时的肠道抗F4反应。

Parenteral vaccination of mice and piglets with F4+ Escherichia coli suppresses the enteric anti-F4 response upon oral infection.

作者信息

Bianchi A T, Scholten J W, van Zijderveld A M, van Zijderveld F G, Bokhout B A

机构信息

DLO-Institute for Animal Science and Health, AB Lelystad, Netherlands.

出版信息

Vaccine. 1996 Feb;14(3):199-206. doi: 10.1016/0264-410x(95)00192-4.

Abstract

We studied with a mouse model and in piglets the requirements to prime for a secondary, mucosal B-cell response against Escherichia coli F4 fimbriae, an important virulence factor of enterotoxigenic E. coli, the agent associated with postweaning diarrhoea in piglets. The major observation obtained with the mouse model was verified for piglets. Mice and piglets were primed orally or parenterally with purified F4ac antigen or whole bacterial cells carrying the F4ac antigen and were later orally infected with live F4ac+ E. coli bacteria. Cell suspensions of murine spleen or porcine serum were used to study the systemic B-cell response. Cell suspensions were also made of murine and porcine enteric lamina propria and were used to study the mucosal B-cell response. Enzyme-linked immunospot assays and enzyme-linked immunosorbent assays specific to E. coli F4ac antigen were used to quantify either the antibody-secreting cells or antibody titres in serum. Results showed that in mice only primary oral immunization with live bacteria induced an enteric immune response against the E. coli F4ac+ fimbriae. Oral immunization with killed bacteria induced hardly any mucosal immune response. Parenteral immunization induced a state of suppression that was reflected by the lack of an enteric immune response upon a subsequent oral infection with live bacteria. A comparable induction of suppression was observed in piglets using the same protocol. We conclude that parenteral vaccination of piglets with the E. coli F4ac antigen is ineffective to induce protective immunity at the mucosal level against postweaning diarrhoea and is possibly detrimental.

摘要

我们使用小鼠模型和仔猪研究了引发针对大肠杆菌F4菌毛的二次黏膜B细胞应答的条件,F4菌毛是产肠毒素大肠杆菌的一种重要毒力因子,该病原体与仔猪断奶后腹泻有关。在小鼠模型中获得的主要观察结果在仔猪中得到了验证。用纯化的F4ac抗原或携带F4ac抗原的全菌细胞经口服或非肠道途径对小鼠和仔猪进行初次免疫,随后经口服感染活的F4ac+大肠杆菌。用小鼠脾脏或猪血清的细胞悬液研究全身性B细胞应答。还制备了小鼠和猪肠道固有层的细胞悬液,用于研究黏膜B细胞应答。使用针对大肠杆菌F4ac抗原的酶联免疫斑点试验和酶联免疫吸附试验来定量血清中的抗体分泌细胞或抗体滴度。结果表明,在小鼠中,仅用活细菌进行初次口服免疫可诱导针对大肠杆菌F4ac+菌毛的肠道免疫应答。用灭活细菌进行口服免疫几乎不诱导任何黏膜免疫应答。非肠道免疫诱导了一种抑制状态,这在随后经口服感染活细菌时肠道免疫应答的缺乏中得到体现出。使用相同方案在仔猪中观察到了类似的抑制诱导现象。我们得出结论,用大肠杆菌F4ac抗原对仔猪进行非肠道疫苗接种在黏膜水平诱导针对断奶后腹泻的保护性免疫方面无效,并且可能有害。

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