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Acidosis is associated with  E. coli  induced pyelonephritis but whether bacterial cell wall constituents inhibit HCO 3  transport in the outer medullary collecting duct from the inner stripe (OMCDi) is not known. We examined the effect of lipopolysaccharide (LPS), on HCO 3  absorption in isolated perfused rabbit OMCDi. LPS caused a ~ 40% decrease in HCO 3  absorption, providing a mechanism for  E. coli  pyelonephritis-induced acidosis. Monophosphoryl lipid A (MPLA), a detoxified TLR4 agonist, and Wortmannin, a phosphoinositide 3-kinase inhibitor, prevented the LPS-mediated decrease, demonstrating the role of TLR4-PI3-kinase signaling and providing proof-of-concept for therapeutic interventions aimed at ameliorating OMCDi dysfunction and pyelonephritis-induced acidosis.

Lipopolysaccharide directly inhibits bicarbonate absorption by the renal outer medullary collecting duct