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Heat shock response enhances acid tolerance of Escherichia coli O157 : H7
Author(s) -
Hong Wang,
Doyle
Publication year - 1998
Publication title -
letters in applied microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.698
H-Index - 110
eISSN - 1472-765X
pISSN - 0266-8254
DOI - 10.1046/j.1472-765x.1998.00264.x
Subject(s) - escherichia coli , chloramphenicol , heat shock , heat shock protein , preservative , strain (injury) , shock (circulatory) , biochemistry , biology , amino acid , enterobacteriaceae , bacteria , hsp70 , chemistry , microbiology and biotechnology , antibiotics , food science , gene , medicine , genetics , anatomy
Escherichia coli O157 : H7 (O157) has unusual acid tolerance. The influence of heat shock on acid tolerance of O157 was studied. Seven strains of O157 and E. coli K‐12 were tested for their ability to survive in minimum glucose medium (pH 2·5) at 37 °C. The survival of heat‐shocked (10 min at 48 °C) cells was about 10–100 times greater compared with untreated cells depending on the strain. No significant difference ( P > 0·05) for O157 strain 932 was observed between heat shock‐induced and acid adaptation‐induced (pH 5·0) acid tolerance. Chloramphenicol prevented heat shock‐induced acid tolerance, indicating the requirement of newly synthesized protein(s). Two outer membrane proteins (OMP) (22 and 15 kDa) were synthesized within 10 min of heat shock and were expressed for at least 6 h by cells held at 37 °C. N‐terminal amino acid sequence analysis suggested that the 22 kDa OMP is a component of an alkyl hydroperoxide reductase. This protein contains a redox active disulphide, which is probably involved in H + transport. Results indicate that sublethal heat treatment of O157 cells substantially increases their tolerance to acidic conditions. This could have practical implications for foods that receive a mild heat treatment and rely on acid as a preservative.