Summary auto-generated
This study compared acetate tolerance in Escherichia coli O157:H7, a pathogenic foodborne strain, and the laboratory strain K-12. E. coli O157:H7 was at least fourfold more resistant to acetate toxicity than K-12 in both batch and continuous cultures at pH 5.9. The key difference lay in intracellular pH regulation: K-12 maintained a constant transmembrane pH gradient (ΔpH) of approximately 0.9 units regardless of acetate concentration, accumulating up to 500 mM intracellular acetate. In contrast, O157:H7 decreased its intracellular pH and ΔpH from 0.9 to 0.2 units as external acetate increased, limiting intracellular acetate to 300 mM. When acetate was added, both strains increased glucose consumption and shifted fermentation end-products to produce more D-lactate, consistent with decreased ATP production rather than uncoupling. The increased D-lactate production in O157:H7 may involve the methylglyoxal shunt, helping lower intracellular pH and prevent toxic acetate anion accumulation. These metabolic differences explain O157:H7's enhanced survival under acidic conditions with acetate, relevant to its persistence in acidified foods and potentially the gastrointestinal tract.
Key findings
- E. coli O157:H7 is at least fourfold more resistant to acetate toxicity than K-12 strain in anaerobic cultures at pH 5.9
- O157:H7 maintains lower intracellular pH and reduced transmembrane pH gradient when exposed to acetate, while K-12 maintains constant high pH gradient
- O157:H7 accumulates less intracellular acetate (maximum 300 mM) compared to K-12 (up to 500 mM) due to differences in pH regulation
- Acetate addition stimulates D-lactate production in both strains, suggesting metabolic shift toward lower ATP yield rather than proton uncoupling
- The acetate tolerance of O157:H7 is explained by fundamental differences in intracellular pH regulation and lactate metabolism, not by enhanced membrane transport mechanisms
This summary was generated automatically from the article PDF and is not part of the original publication. Refer to the PDF for the authoritative text.
Abstract
Batch cultures of Escherichia coli K-12 grew well in an anaerobic glucose medium at pH 5.9, but even small amounts of acetate (20 mM) inhibited growth and fermentation. E. coli O157:H7 was at least fourfold more resistant to acetate than K-12. Continuous cultures of E. coli K-12 (pH 5.9, dilution rate 0.085 h-1) did not wash out until the sodium acetate concentration in the input medium was 80 mM, whereas E. coli O157:H7 persisted until the sodium acetate concentration was 160 mM. E. coli K-12 cells accumulated as much as 500 mM acetate, but the intracellular acetate concentration of O157:H7 was never greater than 300 mM. Differences in acetate accumulation could be explained by intracellular pH and the transmembrane pH gradient (δpH). E. coli K-12 maintained a more or less constant δpH (intracellular pH 6.8), but E. coli O157:H7 let its δpH decrease from 0.9 to 0.2 units as sodium acetate was added to the medium. Sodium acetate increased the rate of glucose consumption, but there was little evidence to support the idea that acetate was creating a futile cycle of protons. Increases in glucose consumption rate could be explained by increases in D-lactate production and decreases in ATP production. Intracellular acetate was initially lower than the amount predicted by ApH, but intracellular acetate and δpH were in equilibrium when the external acetate concentrations were high. Based on these results, the acetate tolerance of O157:H7 can be explained by fundamental differences in metabolism and intracellular pH regulation. By decreasing the intracellular pH and producing large amounts of D-lactate, O157:H7 is able to decrease δpH and prevent toxic accumulations of intracellular acetate anion.