Sublethal concentrations of antibiotics and bacterial adhesion.
Various antibiotics in sublethal concentrations markedly impair adhesion of Streptococcus pyogenes and Escherichia coli to human cells. In streptococcal cells penicillin G caused an enhances loss of lipoteichoic acid, the ligand (adhesion) that binds the organism to host cells, with consequent loss of their adhesive properties. In E coli sublethal concentrations of penicillin prevented the surface expression of the mannose-specific adhesion by distorting cell wall biosynthesis. In contrast to streptococci, E coli cells could not be made to lose their adhesions once their adhesions once they had been formed. Streptomycin in subinhibitory concentration similarly suppressed the acquisition of mannose-binding and adhesive activities in several strains of antibiotic-sensitive E. coli but not in isogenic derivatives with ribosomal mutation to high-level streptomycin resistance, rpsL, or in bacteria in the stationary phase of growth, suggesting that streptomycin exerted its sublethal suppressive effects by classic mechanisms of action on the bacterial ribosome. Strain VL2, derived from one streptomycin-resistant mutant, retained a high level (1000 microgram/ml) of resistance to streptomycin but reacquired sensitivity to the sublethal effect; growth in 30 microgram streptomycin/ml suppressed mannose-sensitive haemagglutination (less than 1% of control) as well as mannose-sensitive adhesion to epithelial cells (42%) or leucocytes (7%). Although these streptomycin-treated bacteria demonstrated an unaltered degree of fimbriation their fimbriae were significantly longer than those on the untreated bacteria. Furthermore, in contrast to the untreated bacteria, the fimbriae isolated from the drug-treated bacteria were found to lack mannose-binding activity as measured by haemagglutination. It therefore, appears that streptomycin can cause even resistant bacteria to produce an aberrant fimbrial protein, presumably by causing misreading in "competent" ribosomes. These studies indicate that the use of sublethal doses of certain antibiotics whose mode of action is well known may shed light on the genetic and chemical modulation of bacterial factors involved in mucosal colonization.
D000268:Adhesiveness; D000900:Anti-Bacterial Agents / Q000494:pharmacology*; D004305:Dose-Response Relationship, Drug; D004848:Epithelium / Q000382:microbiology*; D004926:Escherichia coli / Q000187:drug effects* / Q000502:physiology / Q000648:ultrastructure; D029968:Escherichia coli Proteins; D010861:Fimbriae, Bacterial / Q000378:metabolism; D006801:Humans; D008070:Lipopolysaccharides; D008358:Mannose / Q000378:metabolism; D010400:Penicillin G / Q000494:pharmacology; D010712:Phosphatidic Acids / Q000378:metabolism; D000091243:Ribosomal Protein S9; D013297:Streptococcus pyogenes / Q000187:drug effects* / Q000502:physiology / Q000648:ultrastructure; D013307:Streptomycin; D013682:Teichoic Acids / Q000378:metabolism
D000900:Anti-Bacterial Agents; D029968:Escherichia coli Proteins; D008070:Lipopolysaccharides; D010712:Phosphatidic Acids; D000091243:Ribosomal Protein S9; C000717190:RpsI protein, E coli; D013682:Teichoic Acids; C009900:lipoteichoic acid; D008358:Mannose; D010400:Penicillin G; D013307:Streptomycin