Table 1.
Sources and properties of the main human antimicrobial peptides (AMPs).
| AMPs | Sources | Antimicrobial Spectrum | Immunomodulating Actions | Other Properties |
|---|---|---|---|---|
| Human neutrophil peptides (HNPs) 1 to 4 | Neutrophils | Gram+ and gram- bacteria (S. aureus, bacillus subtilis, S. epidermis, E. coli, P. aeruginosa), fungi (C. albicans), and viruses (influenza v., HSV, CMV) | Induction: TNF-α and IL-1β and chemotaxis (neutrophils, immature Dcs and other immune cells). Inhibition: IL-10. | |
| Human defensins (HDs) 5 & 6 | PCs (HD-5 and -6), epithelia of the female reproductive tract (HD-5) | Gram+ and gram- bacteria (E. coli, Listeria monocytogenes, Salmonella typhimurium, S. aureus), and C. albicans). | Induction: IL-8 and chemotaxis of macrophages, T lymphocytes, and mast cells. | Modulation of the commensal bacteria in the small intestine. |
| Human β-defensins (HBDs) 1 to 4 | Neutrophils and other immune cells, keratinocytes, and epithelia of respiratory, GI, and genitourinary tracts. They can be found in blood, urine, heart, and skeletal muscles (HBD-3), and testis. | HBD-1 to -4: Gram- bacteria (P. aeruginosa, E. coli, vancomycin resistant Enterococcus); HBD-1: anaerobic gram+ bacteria. HBD-2 to -4: Gram+ bacteria (S. aureus, S. Mutans, Str. Pneumoniae, Str. pyogenes) | Induction: pro-inflammatory cytokines, chemotaxis of inflammatory cells, differentiation of monocytes, proliferation and activation of CD4+ T cells, activation of mast cells (release of histamine & PGD2). Inhibition: IL-6 and IL-8 (HBD-3), apoptosis of DCs. Linkage of innate with acquired immunity, activation of the classical complement system pathway. | Preservation of epithelial barrier integrity, amelioration and repair of inflammation-induced tissue injury, antioxidant action. |
| Cathelicidin LL-37 | Immune cells (neutrophils, macrophages, monocytes, B-cells, T-cells), and in most types of epithelial cells (GI, skin, lung, etc.). | Bacteria (E. coli, Listeria monocytogenes, Enterococcus faecium), fungi, and viruses. Synergistic effect with HNP-1, HBD-2, and HBD-3. Inhibition of biofilm formation. | Induction: Production of IL-1β, IL-6, IL-8, and TNF-α, IL-10, and chemokines, chemotaxis of neutrophils, monocytes, and mast cells, monocyte differentiation, macrophage pyroptosis and activation, vascular endothelium proliferation. Suppression: neutrophil apoptosis stimulates bactericidal activity. Inhibits sepsis-induced production of pro-inflammatory cytokines. Binds LPS (antiendotoxin action). | Promotion of angiogenesis, arteriogenesis, and re-epithelialization of wounded epithelia and epidermis. |
| Antileukoprotease elafin | Epithelia (skin, respiratory tract, intestine, endometrium), neutrophils, and macrophages. | S. Aureus, P. aeruginosa, A spergillus fumigatus, and C. albicans. | Promotion of neutrophil and lymphocyte chemotaxis, LPS response, humoral and cellular aspects of adaptive immunity. Inhibition of inflammatory cell recruitment and NF-κB activation. | Inhibition of proteases, promotion of tissue remodeling and cellular differentiation. |
| Antileukoprotease SLPI | Inflammatory cells (neutrophils and macrophages, mast cells), keratinocytes, and epithelial cells of respiratory and GI systems, and amniotic membranes. | Gram+ bacteria (S. aureus and S. epidermidis, group A Streptococcus), Gram- bacteria (E. coli, P. aeruginosa), fungi (Aspergillus fumigatus, C. albicans), and viruses. | Inhibition of inflammatory infiltrate, NF-κB activation, mast cell histamine release, and C5a production. Modulation of adaptive immune responses. | Neutralization of proteases, involvement in cutaneous and oral mucosal wound healing. |
C, Candida; CB, cord blood; DCs, dendritic cells; E, Escherichia; GI, gastrointestinal; P, Pseudomonas; PCs, Paneth cells; S, Staphylococcus; SLPI, secretory leukoprotease inhibiting peptide.