Avoiding dehydration comes with a price, according to Chassin et al. (page 2837). The body's efforts to stay hydrated reduce its ability to fight kidney-invading bacteria.

The body responds to dehydration by producing the hormone vasopressin, which instructs the kidneys to absorb more water. Vasopressin tells cells that line the collecting ducts linking the kidneys to the urinary tract to make more membrane water channels and thus absorb more water. These collecting duct cells are also the targets of Escherichia coli and other intestinal bacteria, which can then enter the kidney and trigger inflammation.

The resulting kidney and urinary tract infections (UTIs) are particularly common in dehydrated individuals. Chassin et al. now find that high levels of vasopressin may be to blame.

Mice that were given vasopressin and later inoculated with bacteria in the urinary tract failed to clear the pathogens. Treatment with a vasopressin antagonist stimulated inflammatory cytokine production and neutrophil recruitment and rapidly reduced the bacterial load. Normally, immunity-promoting cytokines are turned on by the NF-κB pathway when Toll-like receptors recognize bacteria. But vasopressin suppressed their production in collecting duct cells by increasing the levels of phosphatases that inhibit NF-κB activation.

These findings may help explain why drinking more water speeds up recovery from UTIs and kidney infections. The resulting drop in vasopressin levels probably allows a strong antibacterial immune response to be unleashed. But why this antidiuretic hormone has evolved an antiinflammatory function is still a mystery.