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

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