The C. difficile clnRAB operon initiates adaptations to the host environment in response to LL-37

• DOI: 10.1371/journal.ppat.1007153
• Publication Date: 2018-08-20T17:32:46Z
• Authors: Emily C. Woods; Adrianne N. Edwards; Kevin O. Childress; Joshua B. Jones; Shonna M. McBride
• Keywords: Cathelicidin

To cause disease, Clostridioides (Clostridium) difficile must resist killing by innate immune effectors in the intestine, including host antimicrobial peptide, cathelicidin (LL-37). The mechanisms that enable C. to adapt intestine presence of peptides are unknown. Expression analyses revealed an operon, CD630_16170-CD630_16190 (clnRAB), which is highly induced LL-37 and not expressed response other cell-surface active antimicrobials. This operon encodes a predicted transcriptional regulator (ClnR) ABC transporter system (ClnAB), all required for function. Analyses clnR mutant indicate ClnR pleiotropic directly binds controls expression numerous genes, many involved metabolism, cellular transport, signaling, gene regulation, pathogenesis. data suggest ClnRAB novel regulatory mechanism senses as signal regulates intestinal environment during infection.