*3.2. Temporin A*

Temporin A has demonstrated the ability to inhibit the production of TNF-alpha, IL-6, and NO by macrophages in mouse models and is active against antibiotic-resistant Grampositive cocci. Specifically, it has shown efficacy against *Staphylococcus aureus* in mouse models and was particularly high 6 h after injection. The most effective antibiotic used in combination was imipenem (lethality rates of 25% for temporin A, 20% for imipenem, and 10% for temporin A + imipenem). Temporin A is able to facilitate the passage of imipenem across the bacterial membrane by destructuring it, as both act on peptidoglycan. In addition, temporin A appears to induce the migration of human monocytes, neutrophils, and macrophages [40].

#### *3.3. BMAP-28*

BMAP-28 has been shown to inhibit TNF-alpha release and NO production. In mouse models, it has shown similar lethality to antibiotics such as clarithromycin and imipenem against *Staphylococcus aureus*. In addition, it appears to have a superior ability to neutralise bacterial products released by Gram-positive bacteria, a positive factor in severe staphylococcal infections when used in combination with other antimicrobial agents [41].

#### *3.4. Magainin II and Cecropin A*

Magainin II and Cecropin A are two alpha-helical antimicrobial peptides that have demonstrated in vitro activity and in vivo efficacy against *Staphylococcus aureus* with intermediate resistance to glycopeptides in combination with vancomycin. In particular, the combination of magainin II and vancomycin has been shown to be particularly effective in reducing lethality in murine models of staphylococcal sepsis (lethality of 1/20 vs. 6/20 vancomycin vs. 10/20 magainin II vs. 12/20 cecropin A). These two peptides appear to be able to insert into the cytoplasmic membrane and activate murine bacterial hydrolases, resulting in peptidoglycan damage and cell lysis [42].
