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猪胸膜肺炎放线杆菌生物型-血清型之间的交叉保护作用。

Cross-protection between Actinobacillus pleuropneumoniae biotypes-serotypes in pigs.

作者信息

Haesebrouk F, Van de Kerkhof A, Dom P, Chiers K, Ducatelle R

机构信息

Laboratory of Veterinary Bacteriology and Mycology, Faculty of Veterinary Medicine, University of Gent, Merelbeke, Belgium.

出版信息

Vet Microbiol. 1996 Oct;52(3-4):277-84. doi: 10.1016/s0378-1135(96)00075-2.

Abstract

Four groups of hysterectomy-derived and colostrum-deprived pigs were intranasally inoculated with an Actinobacillus pleuropneumoniae biotype 1-serotype 2 strain (producing RTX toxins ApxII and ApxIII. 6 pigs), an A. pleuropneumoniae biotype 1-serotype 10 strain (producing ApxI. 5 pigs), an A. pleuropneumoniae biotype 2-serotype 2 strain (producing ApxII, 5 pigs) or saline (controls, 7 pigs). All pigs were exposed to A. pleuropneumoniae biotype 1-serotype 2 endobronchial challenge. After challenge, severe clinical signs were observed in all control pigs, one pig immunized with the A. pleuropneumoniae biotype 1-serotype 10 strain and two pigs immunized with the A. pleuropneumoniae biotype 2-serotype 2 strain. These pigs died within 36 h after challenge and 20 to 50% of the lungs were macroscopically affected. In the other pigs, clinical signs were mild or absent and no or only small, focal lung lesions were observed when euthanized at 48 h after challenge. At the time challenge neutralizing antibodies against ApxI only. ApxII only and both ApxII and III were present in sera of pigs immunized with the A. pleuropneumoniae biotype 1-serotype 10 strain, the A. pleuropneumoniae biotype 2-serotype 2 strain and the A. pleuropneumoniae biotype 1-serotype 2 strain, respectively. These results indicate that immune mechanisms other than Apx neutralizing antibodies were involved in partial cross-protection of pigs immunized against A. pleuropneumoniae biotype 1-serotype 10 and challenged with the A. pleuropneumoniae biotype 1-serotype 2.

摘要

将四组子宫切除且初乳缺失的猪经鼻接种胸膜肺炎放线杆菌生物1型-血清型2菌株(产生RTX毒素ApxII和ApxIII,6头猪)、胸膜肺炎放线杆菌生物1型-血清型10菌株(产生ApxI,5头猪)、胸膜肺炎放线杆菌生物2型-血清型2菌株(产生ApxII,5头猪)或生理盐水(对照组,7头猪)。所有猪均接受胸膜肺炎放线杆菌生物1型-血清型2支气管内攻毒。攻毒后,所有对照猪、1头用胸膜肺炎放线杆菌生物1型-血清型10菌株免疫的猪和2头用胸膜肺炎放线杆菌生物2型-血清型2菌株免疫的猪出现严重临床症状。这些猪在攻毒后36小时内死亡,且20%至50%的肺在肉眼观察下受到影响。在其他猪中,临床症状轻微或无临床症状,在攻毒后48小时实施安乐死时,未观察到或仅观察到小的局灶性肺部病变。攻毒时,仅针对ApxI、仅针对ApxII以及同时针对ApxII和III的中和抗体分别存在于用胸膜肺炎放线杆菌生物1型-血清型10菌株、胸膜肺炎放线杆菌生物2型-血清型2菌株和胸膜肺炎放线杆菌生物1型-血清型2菌株免疫的猪的血清中。这些结果表明,除Apx中和抗体外,免疫机制也参与了用胸膜肺炎放线杆菌生物1型-血清型10免疫并接受胸膜肺炎放线杆菌生物1型-血清型2攻毒的猪的部分交叉保护作用。

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