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Cefoperazone-treated Mouse Model of Clinically-relevant Clostridium difficile Strain R20291
Published on: December 10, 2016
Secretome analysis of Clostridium difficile strains
Alexander Boetzkes1, Katharina Wiebke Felkel, Johannes Zeiser
1Hannover Medical School, Institute of Toxicology, Carl-Neuberg-Str. 1, 30625 Hannover, Germany.
Archives of Microbiology
|March 9, 2012
Summary
Researchers compared the protein secretomes of Clostridium difficile strains, identifying unique proteins in hypervirulent strains (PCR ribotype 027). This comparative analysis aids in understanding C. difficile virulence factors.
Area of Science:
- Microbiology
- Proteomics
- Infectious Diseases
Background:
- Clostridium difficile causes a spectrum of infections, from mild diarrhea to severe pseudomembranous colitis.
- Emergence of hypervirulent Clostridium difficile strains (PCR ribotype 027) since 2003 has increased mortality rates.
Purpose of the Study:
- To compare the secretomes of three Clostridium difficile strains: CDR20291, CD196, and CD630.
- To identify secreted proteins, particularly those specific to hypervirulent strains.
Main Methods:
- Proteins in the supernatant were separated using SDS-PAGE and analyzed by LC-MS.
- Secreted proteins were predicted using SecretomeP and SignalP.
- Toxins A and B were detected using immunological techniques.
Main Results:
- 158 different proteins were identified in the Clostridium difficile supernatant; most originated from the cytoplasm.
- 32, 36, and 26 secreted proteins were identified in strains CDR20291, CD196, and CD630, respectively.
- The ADP-ribosyltransferase-binding component of binary toxin CDT was identified exclusively in hypervirulent ribotype 027 strains, along with other strain-specific secreted proteins.
Conclusions:
- The study identified numerous secreted proteins across different Clostridium difficile strains.
- Specific secreted proteins, including components of the binary toxin CDT, are associated with hypervirulent strains, offering insights into their increased pathogenicity.
