CAMP (cathelicidin antimicrobial peptide) is a multifunctional innate immune effector with primary antimicrobial activity. The gene encodes a peptide that inhibits growth of gram-negative (E. coli) and gram-positive (B. megaterium) bacteria while exhibiting cytolytic activity against human erythrocytes [UniProt]. CAMP functions as a key component of antibacterial humoral immunity, mediating defense responses through direct antimicrobial mechanisms and neutrophil activation in mucosal tissues [GO annotations]. Beyond its classical antimicrobial role, CAMP is expressed in metabolically active tissues including adipocytes, where it functions as a putative adipokine in metaflammation. TNFα significantly induces CAMP gene expression in mature adipocytes via PI3K signaling, while cell-free DNA impairs expression 1. This suggests CAMP participates in adipose tissue innate immunity and metabolic-immune crosstalk relevant to obesity and cardiovascular disease pathogenesis. CAMP gene expression increases substantially during adipocyte differentiation and shows tissue-specific regulation, with positive correlation between CAMP and TLR9 expression in subcutaneous but not visceral adipose tissue 1. These findings establish CAMP as a dual-function molecule bridging classical antimicrobial defense with metabolic inflammation, positioning it as a potential therapeutic target in obesity-associated immunological dysfunction.