Practice question

Acid tolerance is vital survival strategy for enteric bacteria such as Escherichia coli, Salmonella Typhimurium and Shigella flexneri that must traverse gastric compartment where pH can fall to 1-3 and organic acid stress in intestine. Enterobacteriaceae deploy multiple amino acid decarboxylase antiporter systems for pH homeostasis. Under acidic conditions, inducible decarboxylases such as CadA lysine decarboxylase, AdiA arginine decarboxylase and GadA/B glutamate decarboxylases consume an intracellular proton during decarboxylation of substrate to produce cadaverine, agmatine and gamma-aminobutyrate respectively plus CO2. The more alkaline product is exported via specific antiporters CadB, AdiC and GadC in 1:1 exchange for fresh extracellular substrate, effectively exporting proton equivalents and raising internal pH by up to 0.5 units. CadB-dependent lysine decarboxylation generates cadaverine that additionally blocks outer membrane porins OmpF and OmpC to reduce proton leak. This system raises membrane potential, maintains enzyme function and prevents DNA damage. PhoP-PhoQ senses Mg2+ limitation and antimicrobial peptides, OxyR senses peroxide, SoxR senses superoxide, so acid-specific decarboxylation antiporter module represents the major pH homeostasis strategy underpinning enteric pathogenesis.