β-Oxidation-mediated resistance ofEscherichia coli to inhibition by long-chain fatty acids

Abstract

Decanoate exerted a stronger bactericidal action onEscherichia coli K76 (β-oxidation negative) than on its β-oxidation constitutive parent,E. coli K113; both strains had a normal lipopolysaccharide layer.E. coli RC59, a mutant carrying a defective lipopolysaccharide layer, was more sensitive than its parent,E. coli O111B4, to the growth inhibition by decanoate. Oleate did not affectE. coli RC59 viability, but washing of the cells rendered them sensitive.E. coli RC59 was unable to degrade decanoate and oleate. A mutant of this strain was isolated (E. coli ER20) which retained the defective lipopolysaccharide but was able to metabolize oleic acid. When the killing effect of oleate was assayed on washed cells ofE. coli O111B4, RC59, and ER20, a positive correlation between β-oxidation activity and the number of surviving viable cells was found. The ability of Gram-negative organisms to withstand the toxic effect of fatty acids was attributed to the presence of a lipolysaccharide (LPS) layer in the cell envelope. An additional mechanism of resistance is suggested by the results in this report which show that the ability to oxidize fatty acids contributes to resistance.