Acute pyelonephritis (but not cystitis or "asymptomatic" bacteriuria) due to Escherichia coli induces serum antibodies to O-but rarely to K-antigens, especially not to the most common antigen, K1. Locally produced secretory IgA and IgG antibodies to O-and K-antigens appear in urine during most infections. The E. coli in urine of patients with asymptomatic bacteriuria are different from those in patients with acute pyelonephritis and cystitis and undergo continuous changes, presumably caused by the local antibody response. The E. coli become less virulent and are less able to attach to uroepithelial cells than E. coli causing acute symptomatic infections. Antibodies in urine prevent epithelial adherence. Parenteral and intravesicular injections of killed bacteria can protect against ascending pyelonephritis in rats. A few K-antigens dominate among E. coli that cause urinary tract infections. Vaccination of problem cases is a possibility because of the protective nature of K-antibodies. The mechanism of renal scarring that appears in some patients with urinary tract infections is unknown. Autoantibodies to the Tamm-Horsfall protein that increase after acute pyelonephritis or the cross-reactions noted between certain E. coli and antigens on the kidney may be involved.