Requirement of CRAMP for mouse macrophages to eliminate phagocytosed <i>E. coli</i> through an autophagy pathway

ABSTRACT Host-derived antimicrobial peptides play an important role in the defense against extracellular bacterial infections. However, capacity of derived from macrophages as potential antibacterial effectors intracellular pathogens remains unknown. In this study, we report that normal (wild-type, WT) mouse increased their expression cathelin-related peptide (CRAMP, encoded by Camp) after infection viable E. coli or stimulation with inactivated and its product lipopolysaccharide (LPS), a process involving activation NF-κB followed protease-dependent conversion CRAMP inactive precursor to active form. The was required WT for elimination phagocytosed coli, participation autophagy-related proteins ATG5, LC3-II LAMP-1, well aggregation bacteria p62 (also known SQSTM1). This impaired CRAMP−/− macrophages, resulting retention fragmentation macrophages. These results indicate is critical component autophagy-mediated clearance