Pathogenic bacteria produce surface-associated complex carbohydrate capsules that prevent complement-mediated and antibody-mediated neutralization by the host. However, the capsule is also a major immunogen and a target of antimicrobial peptides (AMPs), so in different host tissues (such as the epithelium), pneumococci shed the capsule by an unknown mechanism. In a recent study, Kietzman et al. showed that exposure to cationic AMPs (CAMPs) on epithelial surfaces leads to the rapid loss of the Streptococcus pneumoniae capsule. This process was dependent on the hydrolytic activity of the pneumococcal cell wall hydrolase LytA, which is involved in both cell density-dependent and β-lactam antibiotic-induced autolysis. Decreased encapsulation in the epithelium was associated with increased bacterial resistance to microbicidal innate defence molecules and promoted invasion of epithelial cells, whereas enhanced encapsulation in the blood protected bacteria from phagocytosis.