Jost B Helen, Billington Stephen J, Trinh Hien T, Bueschel Dawn M, Songer J Glenn
Department of Veterinary Science and Microbiology, University of Arizona, 1117 East Lowell St., Tucson, AZ 85721, USA.
Infect Immun. 2005 Jan;73(1):652-6. doi: 10.1128/IAI.73.1.652-656.2005.
Beta2-toxin, encoded by cpb2, is implicated in the pathogenesis of Clostridium perfringens enteritis. However, cpb2 genes from nonporcine C. perfringens isolates were not always expressed, at least in vitro. Nucleotide sequencing identified atypical cpb2 genes with 70.2 to 70.7% DNA identity to previously identified (consensus) cpb2. Atypical beta2-toxin displayed 62.3% identity and 80.4% similarity to consensus beta2-toxin. No porcine type C isolates (n = 16) and only 3.3% of porcine type A isolates (n = 60) carried atypical cpb2 genes. However, 88.5% of nonporcine isolates carried atypical cpb2 (n = 78), but beta2-toxin was not expressed. Almost half of the nonporcine consensus cpb2 genes (44.4%) carried a frameshift mutation (n = 9), resulting in an absence of beta2-toxin expression. These findings strengthen the role of beta2-toxin in the pathogenesis of enteritis in neonatal pigs. However, the identification of apparently nonexpressed, atypical cpb2 genes raises the question of whether this protein plays the same role in enteritis in other animal species.
由cpb2编码的β2毒素与产气荚膜梭菌肠炎的发病机制有关。然而，来自非猪源产气荚膜梭菌分离株的cpb2基因并非总能表达，至少在体外是这样。核苷酸测序鉴定出与先前鉴定的（一致的）cpb2具有70.2%至70.7%DNA同一性的非典型cpb2基因。非典型β2毒素与一致的β2毒素具有62.3%的同一性和80.4%的相似性。没有猪C型分离株（n = 16），只有3.3%的猪A型分离株（n = 60）携带非典型cpb2基因。然而，88.5%的非猪源分离株携带非典型cpb2（n = 78），但β2毒素未表达。几乎一半的非猪源一致cpb2基因（44.4%）发生了移码突变（n = 9），导致β2毒素不表达。这些发现强化了β2毒素在新生仔猪肠炎发病机制中的作用。然而，鉴定出明显未表达的非典型cpb2基因引发了一个问题，即这种蛋白质在其他动物物种的肠炎中是否发挥相同作用。
