Summary of HNP-1-, hBD-3-, and LL-37-induced suppression of neutrophil apoptosis. The lifetime of neutrophils, terminally differentiated blood cells, is relatively short, and is regulated by various pathogen- and host-derived antiapoptotic and proapoptotic substances [1–14]. Antimicrobial host defense peptides, HNP-1, hBD-3, and LL-37 cannot only destroy bacteria but also potently suppress neutrophil apoptosis, accompanied with the phosphorylation of ERK-1/-2, the downregulation of tBid (an proapoptotic protein) and upregulation of Bcl-x_L (an antiapoptotic protein), and the inhibition of mitochondrial membrane potential change and caspase 3 activity, possibly via the actions on the distinct receptors, the P2Y₆ nucleotide receptor, the chemokine receptor CCR6, and the low-affinity formyl-peptide receptor FPRL1/the nucleotide receptor P2X₇, respectively [23–25]. Suppression of neutrophil apoptosis results in the prolongation of their lifespan and may be advantageous for the host defense against bacterial invasion.