International Journal of Applied Science and Technology

ISSN 2221-0997 (Print), 2221-1004 (Online) 10.30845/ijast

Role of Heat Shock in Survival of Escherichia Coli and its Small Colony Variant IH3 against Acid Stress.
Paramita Basu, Irvin. N. Hirshfield

The mechanism of killing of bacterial cells by low pH is not known. We studied the survival of Escherichia coli at pH 3.0 and in apple cider, which represents organic acid stress. All studies involve the wild type (WT) E. coli K-12 strain HfrH3000, and IH3, a highly acid resistant small colony variant derived from the WT, and were done in Luria-Bertanim (LB) medium at 37oC with log phase cells. The death of these strains occurs in two distinct phases- a rapid early phase followed by a slower death phase suggesting two different mechanisms of cell damage. The evidence indicates that an increase in membrane permeability to small molecules and increased aggregation of cytoplasmic and membrane proteins contribute to acid-induced death in WT. We have also shown that there is a profound increase in lipopolysaccharide (LPS) release from the outer membrane and lowering of intracellular pH in WT cells with incubation in acidic LB or apple cider. IH3 shows much higher survival in low pH, less membrane damage, lower LPS release, lower protein aggregation and better ability to maintain its intracellular pH on exposure to low pH. Moderately heat shocking the WT cells prior to acid exposure resulted in considerable protection against cell death, membrane damage and cellular protein aggregation but pre-heat shocked IH3 does not show extra protection against acid stress. The data indicate that acid kills the WT cells by multiple mechanisms, and that IH3 resists acid-killing due to a strong LPS-outer membrane interaction.

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