[Permeability barrier of bacterial cell envelopes as cause of resistance to antibiotics (author's transl)].
The uptake of antibiotics into bacterial cells depends on the structures and mechanisms involved in general transport of substrates. Because of their different molecular architecture, the distinct layers of the cell envelope differ in permeability. The cell-wall of gram-positive bacteria, which is simply structured, is therefore more permeable to a series of antibiotics than is the gram-negative cell-wall which is built like other biological membranes. The energy dependent uptake of many antimetabolic antibiotics in managed by the selective transport systems of the cytoplasmic membrane. In the case of antibiotics, which are not analogous in structure with metabolites, the dependence of the drug on active transport is less obvious. The uptake of antibiotics may even be influenced by the target-site of the drug in the cytoplasm. An example is the accumulation of aminoglycoside antibiotics which is initiated by binding of the drugs to the ribosome. The autoinduction of aminoglycoside uptake is associated with an increased transport of polyamines. The broad variety of modes of resistance, based on permeability, results from the large number of components involved in the uptake of antibiotics. Resistance of bacteria can depend on alterations of every layer of the cell envelope. The existence of a capsule can cause resistance, as well as the specific loss of protein components of the outer membrane, which are involved in the uptake of special substrates. The exclusion of antimetabolites by the loss of the cognate transport system yields well defined resistance. By contrast, resistance towards a wide variety of unrelated antibiotics results from the uncoupling of energization and transport phenomena. Resistance based on reduced uptake becomes even more complex when the modification of the target site alters the accumulation of antibiotics. Far beyond common mechanisms is the ability of cells to actively excrete antibiotics. Far beyond common mechanisms is the ability of cells to actively excrete antibiotics that have already penetrated. The induction of selective export systems for tetracyclines is not dependent on activities of cell-borne transport systems but is a consequence of the acquisition of resistance plasmids.
D000900:Anti-Bacterial Agents / Q000378:metabolism*; D001419:Bacteria / Q000187:drug effects* / Q000378:metabolism; D001692:Biological Transport; D002463:Cell Membrane Permeability; D002473:Cell Wall / Q000378:metabolism; D003523:Cycloserine / Q000378:metabolism; D004352:Drug Resistance, Microbial; D008070:Lipopolysaccharides / Q000378:metabolism; D010457:Peptidoglycan / Q000032:analysis; D010743:Phospholipids / Q000378:metabolism; D010957:Plasmids; D011135:Polysaccharides, Bacterial / Q000032:analysis; D013754:Tetracyclines / Q000378:metabolism
D000900:Anti-Bacterial Agents; D008070:Lipopolysaccharides; D010457:Peptidoglycan; D010743:Phospholipids; D011135:Polysaccharides, Bacterial; D013754:Tetracyclines; D003523:Cycloserine
Die Penetrationsbarriere der Bakterienzellwand als Ursache der Antibiotikaresistenz.