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Determination of Tolerable Fatty Acids and Cholera Toxin Concentrations Using Human Intestinal Epithelial Cells and BALB/c Mouse Macrophages
Published on: May 30, 2013
Acid tolerance induced by metabolites and secreted proteins, and how tolerance can be counteracted
1Biology Department, University College London, UK.
Abstract:
Several metabolites and salts including glucose, L-glutamate, L-aspartate, FeCl3, KCl and L-proline induce acid tolerance at neutral external pH (pHo) in log phase Escherichia coli. For induction by glucose and L-glutamate, the processes are independent of integration host factor (IHF), H-NS, CysB, ferric uptake regulator (Fur) and RelA. For most of the above, tolerance does not appear if induction occurs and NaCl, sucrose, SDS or DOC are present. For several responses, cAMP inhibits induction. For many established acid tolerance and sensitization processes, including those tolerance responses switched on at pH 5.0 and by glucose, glutamate or aspartate, induction is associated with secretion of extracellular induction proteins. These proteins bring about the response if added to organisms under normally non-inducing conditions. Secreted components also influence inherent acid tolerances and sensitivities. Analysis of some established tolerance responses indicates that induction is a two-stage process, secreted extracellular proteins playing an obligate role in induction. For example, the functioning of the acid-induced medium protein(s) is essential for acid habituation at pHo 5.0. It seems likely that such two-stage mechanisms are essential for many inducible processes in bacteria.
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