IMMUNOHISTOCHEMICAL LOCALIZATION OF IL-8 AND TGF-BETA IN STREPTOCOCCAL GLOMERULONEPHRITIS

Acute poststreptococcal glomerulonephritis (APSGN) is characterized by diffuse glomerular hypercellularity, primarily as a result of accumul ation of neutrophils (exudative glomerulonephritis), increase in intri nsic glomerular cells, and transient pathological mesangial matrix exp ansion. Cytokines and growth factors are supposed to play an important role as mediators of inflammation and as progression factors in vario us renal disorders. Interleukin-8 is a recently described cytokine, de fined as a selective activator and chemoattractant of polymorphonuclea r leukocytes (PMNL) and transforming growth factor (TGF)-beta plays a central role in the accumulation of pathological extracellular matrix in glomerulonephritis. This study analyzed the biopsies of ten patient s with APSGN, using immunohistochemistry (avidin-biotin complex/horser adish peroxidase method) using monoclonal antibodies anti-IL-8, anti-T GF-beta 1, beta 2, beta 3. Controls consisted of non-immune mouse seru m, or anti-TGF-beta preabsorbed with human recombinant TGF-beta. Compa red with normal renal tissue, and minimal change disease, an increased glomerular IL-8 and TGF-beta staining was observed in all of the biop sies. Furthermore, in one patient, we observed a weak deposit of TGF-b eta in tubulointerstitium. Immunoreactive IL-8 and TGF-beta in glomeru li was correlated with light microscopic and clinical features. There was a significant association (P < 0.05), between IL-8 glomerular immu noreactivity and neutrophil infiltration and between TGF-beta glomerul ar staining and mesangial matrix expansion. Otherwise, there was no co rrelation with the mesangial cellularity. It was concluded that increa sed protein expression of IL-8 and TGF-beta are observed in APSGN and may play a role in the acute glomerular inflammation.