文献类型: 外文期刊
作者: Peng, Wei 1 ; Yang, Xia 1 ; Yan, Kang 1 ; Chen, Huanchun 1 ; Yuan, Fangyan 3 ; Bei, Weicheng 1 ;
作者机构: 1.Huazhong Agr Univ, Coll Vet Med, State Key Lab Agr Microbiol, Wuhan, Peoples R China
2.State Key Lab Genet Engn Vet Vaccines, Qingdao, Peoples R China
3.Hubei Acad Agr Sci, Inst Anim Husb & Vet Sci, Minist Agr, Key Lab Prevent & Control Agents Anim Bacteriosis, Wuhan, Peoples R China
4.Huazhong Agr Univ, Cooperat Innovat Ctr Sustainable Pig Prod, Wuhan, Peoples R China
关键词: Actinobacillus pleuropneumoniae; CopA; copper efflux; copper resistance
期刊名称:VETERINARY MICROBIOLOGY ( 影响因子:3.293; 五年影响因子:3.599 )
ISSN: 0378-1135
年卷期: 2021 年 258 卷
页码:
收录情况: SCI
摘要: Actinobacillus pleuropneumoniae is a Gram-negative bacterium causing porcine pleuropneumonia and severe economic losses in the global swine industry. The toxic trace element copper is required for many physiological and pathological processes in organisms. However, CopA, one of the most well-characterized P-type ATPases contributing to copper resistance, has not been characterized in A. pleuropneumoniae. We used quantitative PCR analysis to examine expression of the copA gene in A. pleuropneumoniae and investigated sequence conservation among serotypes and other Gram-negative bacteria. Growth characteristics were determined using growth curve analyses and spot dilution assays of the wild-type strain and a /copA mutant. We also used flame atomic absorption spectrophotometry to determine intracellular copper content and examined the virulence of the /copA mutant in a mouse model. The copA expression was induced by copper, and its nucleotide sequence was highly conserved among different serotypes of A. pleuropneumoniae. The amino acid sequence of CopA shared high identity with CopA sequences reported from several Gram-negative bacteria. Furthermore, the /copA mutant exhibited impaired growth and had higher intracellular copper content compared with the wild-type strain when supplemented with copper. The mouse model revealed that CopA had no influence on the virulence of A. pleuropneumoniae. In conclusion, these results demonstrated that CopA is required for resistance of A. pleuropneumoniae to copper and protects A. pleuropneumoniae against copper toxicity via copper efflux.
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