In order to investigate the role of bacterial infection in the mediati
on of interstitial scarring, we examined the effect of Escherichia col
i-tubular cell interaction products (ECS) and control tubular cell pro
ducts (CS) on rat renal medullary interstitial cell (RMIC) proliferati
on and collagen accumulation. ECS enhanced (p < 0.001) RMIC proliferat
ion when compared with CS and media alone. ECS, at concentrations of 5
, 10, 15, 20, and 25%, increased (p < 0.001) RMIC proliferation, where
as at higher concentrations (30-70%), ECS attenuated (p < 0.001) RMIC
proliferation when compared with CS and media alone. ECS-induced RMIC
proliferation was attenuated (p < 0.001) by interleukin-6 antibody (EC
S 31,800 +/- 230; ECS + interleukin-6 antibody 16,400 +/- 120 cells/we
ll). ECS at concentrations of 20 and 30% enhanced (p < 0.001) RMIC col
lagen type III accumulation. Transforming growth factor beta antibody
attenuated (p < 0.001) RMIC collagen accumulation induced by ECS (ECS
157 +/- 8; ECS + transforming growth factor beta antibody 83 +/- 10 ng
/mg cellular protein). Moreover, ECS also increased mRNA expression of
transforming growth factor beta in RMIC as compared with CS and media
. The present in vitro study provides a basis for speculation that bac
teria-tubular cell interaction may contribute to the development of in
terstitial scarring.