In S. aureus, rather than cause gross membrane changes, HNP-1 (de Leeuw et al. 2010) and hBD3 (Sass et al. 2011) appear to interfere with cell wall biosynthetic pathways by binding to Lipid II (undecaprenylpyrophosphate-MurNAc[pentapeptide]-GlcNAc), an essential precursor of bacterial cell walls and the target of several antibiotics (Breukink & de Krujiff 2007). The transformation of monomeric lipid II into a polymeric peptidoglycan by the bifunctional S. aureus enzyme Penicillin-binding protein 2 (PBP2) is inhibited by hBD3 (Sass et al. 2011) resulting in local lesions of the cell wall layer through which membranes and cytoplasmic contents ultimately protrude.
Breukink, E, Zeng, P, Li, C, Li, C, Lu, WY, Diepeveen-de Buin, M, Lu, W, de Leeuw, E
Schneider, T, Novikova, N, Tossi, A, Wilmes, M, Shamova, O, Sahl, HG, Körner, C, Sass, V
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