Lysis and aberrant morphology of Bacillus subtilis cells caused by surfactants and their relation to autolysin activity

Abstract

The surfactants tested in this study lysed Bacilus subtilis 168 cells at the logarithmic growth phase. Results obtained with inhibitors and a mutant that had defective autolytic enzymes suggested that cell lysis resulted from the deregulation of autolysin activity. The addition of surfactants at sublytic concentrations produced twisted cells, filamented cells, or both. Autolysins extracted with 5 M LiCl from the cell wall fraction and lysozyme added to cells that were treated with surfactants restored the apparently normal cell rod morphology, suggesting that surfactants interfere with the role of autolysins in normal construction of the cell envelope. The rates of cellular autolysis and autolysin activity remaining in growing cells after exposure to a surfactant at a sublytic concentration decreased, although the rate of turnover of cell wall peptidoglycan was the same as that of control cells. Surfactants were suggested to interact with the regulatory system of autolysins and, thus, to affect the activities of autolysins in B. subls cells and to cause either morphological changes or cell autolysis, depending on the concentration of surfactants.

Lysis of Red Blood Cells and Alveolar Epithelial Toxicity by Therapeutic Pulmonary Surfactants

“…1 and 2). Previous work done by others indicates that some surfactants have a toxic effect on cell membranes (15) ranging from decreased cell viability due to loss of solute-barrier properties of the cell membrane (16) to complete cell lysis (17,18). These observations are surfactant concentration dependent, with low concentrations associated with decreased cell viability and higher concentrations associated with cell lysis.…”

Phenotypes of Bacillus subtilis mutants lacking multiple class A high-molecular-weight penicillin-binding proteins

“…Bending of B. subtilis cells has previously been found to result from a variety of causes, including mutations affecting autolysin activity (5), Triton X-100 resistance (33), or PBPs 2a, 2b, and 3 (26) and treatment of cells with surfactants (35), fatty acid esters (34), local anesthetics (33), penicillin G (33), or electric fields (25). In some cases, this bending has been clearly associated with a decrease in autolytic activity (5,35), suggesting that it may be due to a perturbation of the balance between peptidoglycan synthetic and degradative processes. Obviously, loss of peptidoglycan synthetic activities associated with class A high-molecular-weight PBPs could also produce such an imbalance.…”

Differential Assay for High-Throughput Screening of Antibacterial Compounds

“…Relevant examples include (1) activation of LytA, the principal autolytic enzyme in Streptococcus pneumoniae R6 by penicillin action, 11,13,14 and (2) activation of S. pneumoniae LytA by the action of lysozyme. 10 Moreover, activation of autolysins of B. subtilis 168, by fatty acids 15 and TX-100, 16 has been described.…”

“…4,[10][11][12][13][14][15][16] This was verified under our test conditions by growing cells to A660 = 0.4, at which time, cephalexin, lysozyme, or TX-100 was added. Results shown in Figure 4 FIG.…”