胸膜肺炎放线杆菌ApxI毒素基因突变致弱株的构建及免疫原性分析.pdf

Abstract Actinobacillus a causative of pleuropneumoniae(APP)ispathogenporcineplanropneumonia．In this mutants achievedinsertional dissertation，the serovar10 inactivationof ofA．pleuropneumoniaeby and deletionof constructed weTe bymeansof apxlCgene partial apxL4gene successfully genetic ofthemutantswas studies engineeringtechnique，respectively．Theimmunogenicity analyzed．Our foundationfor aUenuatedlivevaccinewith differentAPP provide developing cross-protectionagainst SemVars． A2．8kb the was fromAPPserovar1 0 DNA fragmentcontainingapxlCgene amplified genomie PCR．Basedon and Xholsiteofthe wasinsertedwitha by cloningsequencing，the apxlCgene resistancecassetceandthetransfer wasconstructed．The chlorarrIphenicolgene plasmidpUIC—Chl7 transfer wasintroducedintothe APPserovar10for plasmid electrocompetent homologous recombination mutant identifiedPeRand strain，termedD13039C’Chg,was byelectroporation．The by Southern mutantwas identicaltothe strain thatitshowedno blotting．The phenotypically parent except able toxin mutantwas tosecretthesame likethe strain．Virulence haemolyticactivity．The Apxl parent ofthemutant at least straindecreased 100fold withthe strain．The