PROTECTIVE ANTIIDIOTYPE ANTIBODIES IN THE PRIMATE MODEL OF PYELONEPHRITIS

The adherence of P-fimbriated Escherichia coli to a receptor containin g alpha-D-Gal-(1-4)-beta-D-Gal (Gal-Gal) on urothelial cells is an imp ortant pathogenic mechanism in the development of pyelonephritis. Anti bodies (Ab1) that had been produced by immunization with Gal-Gal conju gated with bovine serum albumin were specifically purified and used to stimulate the production of anti-idiotypic antibodies (Ab2) in cynomo lgus monkeys (Macaca fascicularis). While sera from all of the Ab2-pro ducing monkeys contained antibodies reactive with Ab1 and P-fimbriae, not all of the sera inhibited P-fimbrial binding to the Gal-Gal recept or. On the basis of the inhibition of binding, Ab2-producing monkeys w ere divided into two groups, termed reactive and nonreactive. The reac tive and nonreactive Ab2-producing monkeys, together with a group of c ontrol monkeys, were challenged with a renal inoculation with P-fimbri ated Escherichia coli. Hematologic, immunologic, microbiologic, and pa thologic data were compared among the three groups. The reactive monke ys, whose Ab2 in serum inhibited binding between P-fimbriae and the Ga l-Gal receptor, were protected against renal damage compared with the control group. The nonreactive group shared some parameters with the r eactive group but overall developed renal damage comparable to that of the controls.