Abstract

We have previously shown a significant increase in 35SO4 uptake in rat GBM when glomeruli were cocultured with PBMC from MLN patients in relapse, but an uptake no different than normal controls if glomeruli were incubated with PBMC of patients in remission. We have studied the 35SO4 uptake by GBM after PBMC from 12 MLN patients in remission have been stimulated with ConA (10 μg/ml of culture media).There was a significant increase in 35SO4 GBM uptake when glomeruli were cocultured with ConA stimulated MLN PBMC (geometric mean [GM], 331 cpm/mg dry glomerular weight) as compared to glomeruli cocultured with MLN PBMC (GM, 200) (P=0.047); glomeruli alone (GM, 162) (p=0.008), and glomeruli alone stimulated with ConA (GM, 146) (p=0.003). No significant differences were seen between the groups when glomeruli were cocultured with PBMC from 12 normal adults (GM range 81-162).These data show that ConA stimulated PBMC from MLN patients in remission alter the sulfate metabolism of rat GBM. The stimulation of PBMC with ConA reproduces the increase in 35SO4 uptake observed when glomeruli are cocultured with PBMC from MLN patients in relapse. Since sulfated compounds in the GBM may play a role in glomerular permeability, these findings suggest that PBMC may play a role in the pathogenesis of this disease by altering the metabolism of GBM sulfated compounds.

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