Table 3.
Kind of Activity | Mechanism of Action | [Ref.] |
---|---|---|
Antibacterial | - Reducing the concentration of iron ions that are necessary to bacterial growth and proliferation (chelation of iron via LF) - Interacting with lipoteichoic acid (LTA) of the cell walls of G(+) bacteria, disintegrating them and increasing their permeability |
[102,115,116] |
- Binding to lipopolysaccharide (LPS) of the walls of G(−) bacteria and disintegrating them. | ||
Antifungal | - Damaging cell membranes of fungi and altering their permeability | [117,118,119] |
- Sequestration of iron | ||
- Membrane destabilization | ||
Antiviral | - Blocking the host’s cell surface receptors due to the LF’s affinity for glycosaminoglycans- Direct interacting with capsid or viral envelope proteins | [113,120,121] |
Antiparasitic | - Targets the host cell entry | [122,123,124,125,126] |
- Sequestration of iron- Probably linked to sequestration of iron | ||
- Acts additively or synergistically with the antiparasitic compounds used in therapy | ||
Antioxidant | - Inhibiting the propagation of hydroxyl radicals by sequestering cationic iron and copper | [109,115,127] |
Anticancer | - Reducing the production of tumor necrosis factor (TNF)-α in cell cultures | [104] |
Immunomodulatory | - Stimulating the phagocytic activity of multinucleated leukocytes | [98,103,104] |
- Reducing the production of interleukin (IL) -6 in cell cultures | ||
- T-cell maturation | ||
- Stimulation of NK (natural killer cells) cells | ||
- Reducing pro-inflammatory cytokines |