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Rice, J.C. et al.

Rice, Spence, Megyesi, Goldblum, Safirstein,

Expression of the polymeric immunoglobulin receptor and excretion of secretory IgA in the postischemic kidney.

The humoral mucosal immune response of the kidney involves the transport of secretory IgA (S-IgA) through renal epithelial cells by the polymeric immunoglobulin receptor (pIgR). The pIgR is cleaved and released as free secretory component (FSC) or attached to IgA (S-IgA). We examined the effects of an ischemic model of acute renal failure (ARF) on the expression of pIgR and the secretion of FSC and S-IgA in the urine. Kidney pIgR mRNA levels decreased in ischemic animals by 55% at 4 h and by 85% at 72 h compared with controls. pIgR protein expression in the medullary thick ascending limb (TAL) decreased within 24 h and was nearly undetectable by 72 h. Urinary S-IgA and FSC concentrations decreased by 60% between days 3 and 6. pIgR mRNA and pIgR protein in the kidney returned to approximately 90% of control levels and urinary FSC and S-IgA concentrations returned to approximately 55% of control levels by day 7. We demonstrate that ischemic ARF decreases renal mucosal S-IgA transport in vivo and may contribute to the increased incidence of urinary tract infections.[1]

References

Expression of the polymeric immunoglobulin receptor and excretion of secretory IgA in the postischemic kidney. Rice, J.C., Spence, J.S., Megyesi, J., Goldblum, R.M., Safirstein, R.L. Am. J. Physiol. (1999) [Pubmed]

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