English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Antimicrobial peptides are essential to the innate immune defense of the mammal against bacterial infection. However, pathogenic bacteria have evolved multiple strategies to resist and evade antimicrobial peptides, which is vital to bacterial survival and colonization in hosts. PR-39 is a linear porcine antimicrobial peptide containing 39 amino acid residues with a high proline content. Resistance to antimicrobial peptide PR-39 has been observed in  Actinobacillus pleuropneumoniae . However, little is known about the factors required for this resistance. In the present study, PR-39 exposure increased the expression of the  sapA  gene in  A. pleuropneumoniae . The  sapA  gene, which encodes a putative peptide transport periplasmic protein, was deleted from this bacterium. The Δ sapA  mutant showed increased sensitivity to PR-39 compared to the wild-type MD12 and complemented PΔ sapA  strains. However, the Δ sapA  mutant did not exhibit any alterations in outer membrane integrity. Scanning electron microscopy showed that the Δ sapA  mutant displayed morphological defects, as indicated by a deformed and sunken shape after PR-39 treatment. In addition, disruption of the SapA protein led to reduced colonization and attenuated virulence of  A. pleuropneumoniae  in the BALB/c mouse model. Collectively, these data suggest that SapA acts as one mechanism for  A. pleuropneumoniae  to counteract PR-39-mediated killing. To the best of our knowledge, this is the first study to show a mechanism underlying antimicrobial peptide resistance in  A. pleuropneumoniae .

The SapA Protein Is Involved in Resistance to Antimicrobial Peptide PR-39 and Virulence of Actinobacillus pleuropneumoniae