The Relationship of Adhesion Molecules and Leukocyte Infiltration in Chronic Tubulointerstitial Nephritis Induced by Puromycin Aminonucleoside in Wistar Rats

• Published in: Clinical immunology and immunopathology Vol. 79; no. 3; pp. 229 - 235
• Main Authors: Wu, Jing-chuan, Fan, Gian-min, Kitazawa, Kozo, Sugisaki, Tetsuzo
• Format: Journal Article
• Language: English
• Published: San Diego, CA Elsevier Inc 01.06.1996; New York, NY Academic Press; Boston
• Subjects: Animals; Biological and medical sciences; Cell Adhesion Molecules - physiology; Chronic Disease; Female; Immunoenzyme Techniques; Intercellular Adhesion Molecule-1 - metabolism; Kidney Tubules - metabolism; Lymphocyte Function-Associated Antigen-1 - metabolism; Medical sciences; Nephritis, Interstitial - chemically induced; Nephrology. Urinary tract diseases; Nephropathies. Renovascular diseases. Renal failure; Nephrotic Syndrome - chemically induced; Puromycin Aminonucleoside - toxicity; Rats; Rats, Wistar; Time Factors; Tubulopathies; Urinary system disease; Rat; Leukocyte; Pathogenesis; Rodentia; Cell adhesion molecule; Biological marker; Renal disease; Adhesion; Vertebrata; Experimental disease; Mammalia; Animal; Tubulointerstitial nephritis
• ISSN: 0090-1229; 1090-2341
• DOI: 10.1006/clin.1996.0073

We studied the expression of adhesion molecules on infiltrating leukocytes and tubular cells in chronic tubulointerstitial nephritis associated with puromycin aminonucleoside (PA) nephrosis. Rats received injections of PA (2 mg/100 g body wt) weekly for the first 3 weeks and every other week thereafter. Rats were killed at 0, 3, 5, 8, and 12 weeks after the start of injections. From the third to the fifth week, the initial infiltrating cells in interstitial tissue were mainly CD4+T lymphocytes. At the fifth week, ICAM-1, CD44, and hyaluronate were expressed on infiltrating cells in interstitial tissue. At the eighth week, the number of infiltrating cells reached a peak and consisted of T lymphocytes (CD4, CD8) and macrophages (ED1, MHC class II, CD11b, and CD18). The severity of interstitial infiltration was correlated with the degree of proteinuria and with ICAM-1 expression. Our results suggest that CD4+T lymphocytes may contribute to the production of initial tubular injury. Expression of ICAM-1 helps mononuclear cells migrate to the interstitium. In addition, expression of CD44 and hyaluronate may play important roles in the chronicity of tubulointer- stitial nephritis.