ArticleInfection and immunity2011
Identification of a genetic locus responsible for antimicrobial peptide resistance in Clostridium difficile.
Article in Infection and immunity, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers.
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Who cites it
88 citing papers in PubMed, 127 citations in OpenAlex.
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- A metabolite dehydrogenase pathway represses sporulation of Clostridioides difficile.Anaerobe · 2025Article
- Antimicrobial peptide-based strategies to overcome antimicrobial resistance.Archives of microbiology · 2024Review
- A nisin-inducible chromosomal gene expression system based on ICE Tn5253 of Streptococcus pneumoniae, transferable among streptococci and enterococci.World journal of microbiology & biotechnology · 2024Article
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- Identification of DraRS inJournal of bacteriology · 2023Article
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- The RgaS-RgaR two-component system promotes Clostridioides difficile sporulation through a small RNA and the Agr1 system.PLoS genetics · 2023Article
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- Article
- Review
- Different CprABC amino acid sequences affect nisin A susceptibility in Clostridioides difficile isolates.PloS one · 2023Article
28 more citing papers are in PubMed but not listed here.
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Clostridium difficile causes chronic intestinal disease, yet little is understood about how the bacterium interacts with and survives in the host. To colonize the intestine and cause persistent disease, the bacterium must circumvent killing by host innate immune factors, such as cationic antimicrobial peptides (CAMPs). In this study, we investigated the effect of model CAMPs on growth and found that C. difficile is not only sensitive to these compounds but also responds to low levels of CAMPs by expressing genes that lead to CAMP resistance. By plating the bacterium on medium containing the CAMP nisin, we isolated a mutant capable of growing in three times the inhibitory concentration of CAMPs. This mutant also showed increased resistance to the CAMPs gallidermin and polymyxin B, demonstrating tolerance to different types of antimicrobial peptides. We identified the mutated gene responsible for the resistance phenotype as CD1352. This gene encodes a putative orphan histidine kinase that lies adjacent to a predicted ABC transporter operon (CD1349 to CD1351). Transcriptional analysis of the ABC transporter genes revealed that this operon was upregulated in the presence of nisin in wild-type cells and was more highly expressed in the CD1352 mutant. The insertional disruption of the CD1349 gene resulted in significant decreases in resistance to the CAMPs nisin and gallidermin but not polymyxin B. Because of their role in cationic antimicrobial peptide resistance, we propose the designation cprABC for genes CD1349 to CD1351 and cprK for the CD1352 gene. These results provide the first evidence of a C. difficile gene associated with antimicrobial peptide resistance.
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