Wiedemann B, Pfeifle D, Wiegand I, Janas E
Pharmazeutische Mikrobiologie, University of Bonn, Bonn, Germany.
Drug Resist Updat. 1998;1(4):223-6. doi: 10.1016/s1368-7646(98)80002-2.
beta-Lactams with the ability to induce beta-lactamase in gram-negative bacteria bind to essential penicillin-binding proteins (PBPs) after entering the periplasmic space. This leads to inactivation of transpeptidase activities and thereby a decrease in the number of peptide cross-links, allowing further degradation of murein by soluble lytic transglycosylases. If all DD-carboxypeptidases (PBP 4, 5, 6a and 6b) are inhibited as well, the degradation product aD-pentapeptide (N-acetylglucosaminyl-1,6-anhydro-N-acetylmuramyl-L-alanyl-D-glutamyl-meso-diaminopimelic-acid-D-alanyl-D- alanine) accumulates, which is the case with inducing beta-lactams such as imipenem. These molecules in addition to tri- and tetrapeptides (N-acetylglucosaminyl-1,6-anhydro-N-acetylmuramyl-L-alanyl-D-glutamyl-meso-diaminopimelic-acid-[D-alanine]) which are the usual degradation products of peptidoglycan, are released into the cytoplasm and displace the UDP-pentapeptide (UDP-N-acetylmuramyl-L-alanyl-D-glutamyl-meso-diaminopimelic-acid-D-alanyl-D-alanine) from the DNA-binding protein AmpR, converting it into an activator of AmpC beta-lactamase expression.
能够诱导革兰氏阴性菌产生β-内酰胺酶的β-内酰胺类药物进入周质空间后会与必需的青霉素结合蛋白(PBPs)结合。这会导致转肽酶活性失活,从而使肽交联数量减少,使得可溶性溶菌转糖基酶能够进一步降解胞壁质。如果所有的DD-羧肽酶(PBP 4、5、6a和6b)也受到抑制,降解产物α-D-五肽(N-乙酰葡糖胺基-1,6-脱水-N-乙酰胞壁酰-L-丙氨酰-D-谷氨酰-内消旋二氨基庚二酸-D-丙氨酰-D-丙氨酸)就会积累,亚胺培南等诱导型β-内酰胺类药物就是这种情况。除了作为肽聚糖常见降解产物的三肽和四肽(N-乙酰葡糖胺基-1,6-脱水-N-乙酰胞壁酰-L-丙氨酰-D-谷氨酰-内消旋二氨基庚二酸-[D-丙氨酸])外,这些分子会释放到细胞质中,并将UDP-五肽(UDP-N-乙酰胞壁酰-L-丙氨酰-D-谷氨酰-内消旋二氨基庚二酸-D-丙氨酰-D-丙氨酸)从DNA结合蛋白AmpR上置换下来,并将其转化为AmpCβ-内酰胺酶表达的激活剂。