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Published on: January 27, 2021
Outer Membrane Lipoprotein Lip40 Modulates Adherence, Colonization, and Virulence of Actinobacillus pleuropneumoniae
Jinlin Liu1, Yurou Cao1, Lulu Gao1
1Hubei Key Laboratory of Genetic Regulation and Integrative Biology, College of Life Sciences, Central China Normal University, Wuhan, China.
Abstract:
Bacterial lipoproteins are a set of membrane proteins with various functions; many of which are virulence factors of pathogenic bacteria. In the present study, we investigated the role of an outer membrane lipoprotein Lip40 in the pathogenesis of Actinobacillus pleuropneumoniae. A mutant strain (Δlip40) lacking Lip40 and a complemented strain (CΔlip40) were constructed. Δlip40 exhibited reduced adherence to the St. Jude porcine lung cells. The ability of the Δlip40 mutant to colonize the mouse lung tissues was significantly impaired compared to that of the wild type and complementation strains. Furthermore, an infection assay revealed that pigs infected with Δlip40 showed fewer clinical signs and lung lesions, indicating that Lip40 contributed to the development of porcine pleuropneumonia. Collectively, our data suggest that Lip40 is involved in the virulence of A. pleuropneumoniae.
Insights
The outer membrane lipoprotein Lip40 is crucial for the virulence of Actinobacillus pleuropneumoniae. Deleting Lip40 significantly reduced bacterial colonization and disease severity in pigs, highlighting its role in pathogenesis.
Area of Science:
- Bacteriology
- Microbial Pathogenesis
- Veterinary Medicine
Background:
- Bacterial lipoproteins are essential membrane proteins with diverse roles.
- Many lipoproteins function as virulence factors in pathogenic bacteria.
- Actinobacillus pleuropneumoniae causes significant economic losses in the swine industry.
Purpose of the Study:
- To investigate the role of the outer membrane lipoprotein Lip40 in the pathogenesis of Actinobacillus pleuropneumoniae.
- To determine Lip40's contribution to bacterial adherence, colonization, and disease development.
Main Methods:
- Construction of a Lip40-deficient mutant (Δlip40) and a complemented strain (CΔlip40) of A. pleuropneumoniae.
- In vitro adherence assays using St. Jude porcine lung cells.
- In vivo colonization studies in mouse lungs.
- Infection assays in pigs to evaluate clinical signs and lung lesions.
Main Results:
- The Δlip40 mutant showed significantly reduced adherence to porcine lung cells compared to the wild type.
- Bacterial colonization of mouse lung tissues was markedly impaired in the Δlip40 mutant.
- Pigs infected with the Δlip40 mutant exhibited fewer clinical signs and reduced lung lesions.
Conclusions:
- Lipoprotein Lip40 is a significant virulence factor for Actinobacillus pleuropneumoniae.
- Lip40 plays a critical role in bacterial adherence, colonization, and the development of porcine pleuropneumonia.
- Targeting Lip40 could be a potential strategy for controlling A. pleuropneumoniae infections.
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