TY - JOUR
T1 - Intercellular adhesion molecule-1, intercellular adhesion molecule-3, and leukocyte integrins in leukocyte accumulation in membranoproliferative glomerulonephritis type I
AU - Soma, Jun
AU - Saito, Takao
AU - Ootaka, Tetsuya
AU - Sato, Hiroshi
AU - Abe, Keishi
N1 - Funding Information:
From The Second Department of Internal Medicine, hoku University School of Medicine, Sendai, Japan. Received December 14, 1995; accepted in revised form July 8, 1996. Supported by a research grant from the Miyagi Prefecture Kidney Association, Japan. Presented in part at the 27th Annual Meeting of the American Society of Nephrology, October 1994, Orlando, FL. Address reprint requests to Jun Soma, MD, The Second Department of Internal Medicine, Tohoku University School of Medicine, I-l, Seiryo-cho, Aoba-ku, Sendai, 980-77, Japan. 0 1996 by the National Kidney Foundation, 0272~6386/96/2805-0004$3.00/O
PY - 1996/11
Y1 - 1996/11
N2 - Marked intraglomerular infiltration of leukocytes is observed in membranoproliferative glomerulonephritis (MPGN). We recently demonstrated that this leukocyte infiltration develops partly through macrophage-1 (Mac- 1)-positive cells and glomerular C3c deposits (Clin Exp Immunol 100:269-276, 1995). To further investigate the mediation of adhesion molecules in the leukocyte accumulation, we immunohistochemically examined the expression of intraglomerular leukocyte integrins and their ligands as wall as surface markers for granulocytes/monocytes (CD15) and macrophages (CD68} in 26 patients with MPGN type I who had undergone repeated biopsies. These patients were divided into two groups. Group A included the patients who showed both normo-complementemia and urinary protein excretion less than 1 g/d at the follow-up biopsy (recovery group: n = 14). Group B (persistent group: n = 12) included the patients other than those in group A. At the initial biopsy, there was no difference in the degree of glomerular C3c deposition, glomerular intercellular adhesion molecule (ICAM)-1 expression, or the numbers of cells bearing leukocyte function-associated antigen-1 (LFA-1), Mac-1, and ICAM-3 between the two groups. At the follow-up biopsy, the degree of glomerular C3c deposition, and the numbers of cella bearing LFA-1, Mac-1, and ICAM-3, were significantly decreased only in group A (P < 0.01, P < 0.001, P < 0.001, and P < 0.01, respectively). No chronological change in ICAM-1 expression was observed in either group. Group B showed a chronological increase in the severity of glomerular injury and serum creatinine level, associated with persistent heavy proteinuria. Neither LFA- 1- nor Mac-1-positive cells were positively correlated with ICAM-1 expression. Most of Mac-1-positive cells were CD15-positive cells (granulocytes/monocytes), and a considerable number of Mac-1-positive cells concurrently expressed ICAM-3. In contrast, most LFA-1-positive cells were considered to be CD68-positive cells (macrophages). The number of cells bearing LFA-1 was positively correlated with that of cells bearing ICAM-3 (P <: 0.00001). These results suggest that the glomerular leukocytes, infiltrating through Mac-1/complement interaction, express ICAM-3 by themselves, and that LFA-1/ICAM-3 interaction might participate in the glomerular aggregation of leukocytes in MPGN type I. In this study, we could not conclude that LFA-1/ICAM-1 or Mac-1/ICAM-1 interaction was involved in the leukocyte accumulation in this disease.
AB - Marked intraglomerular infiltration of leukocytes is observed in membranoproliferative glomerulonephritis (MPGN). We recently demonstrated that this leukocyte infiltration develops partly through macrophage-1 (Mac- 1)-positive cells and glomerular C3c deposits (Clin Exp Immunol 100:269-276, 1995). To further investigate the mediation of adhesion molecules in the leukocyte accumulation, we immunohistochemically examined the expression of intraglomerular leukocyte integrins and their ligands as wall as surface markers for granulocytes/monocytes (CD15) and macrophages (CD68} in 26 patients with MPGN type I who had undergone repeated biopsies. These patients were divided into two groups. Group A included the patients who showed both normo-complementemia and urinary protein excretion less than 1 g/d at the follow-up biopsy (recovery group: n = 14). Group B (persistent group: n = 12) included the patients other than those in group A. At the initial biopsy, there was no difference in the degree of glomerular C3c deposition, glomerular intercellular adhesion molecule (ICAM)-1 expression, or the numbers of cells bearing leukocyte function-associated antigen-1 (LFA-1), Mac-1, and ICAM-3 between the two groups. At the follow-up biopsy, the degree of glomerular C3c deposition, and the numbers of cella bearing LFA-1, Mac-1, and ICAM-3, were significantly decreased only in group A (P < 0.01, P < 0.001, P < 0.001, and P < 0.01, respectively). No chronological change in ICAM-1 expression was observed in either group. Group B showed a chronological increase in the severity of glomerular injury and serum creatinine level, associated with persistent heavy proteinuria. Neither LFA- 1- nor Mac-1-positive cells were positively correlated with ICAM-1 expression. Most of Mac-1-positive cells were CD15-positive cells (granulocytes/monocytes), and a considerable number of Mac-1-positive cells concurrently expressed ICAM-3. In contrast, most LFA-1-positive cells were considered to be CD68-positive cells (macrophages). The number of cells bearing LFA-1 was positively correlated with that of cells bearing ICAM-3 (P <: 0.00001). These results suggest that the glomerular leukocytes, infiltrating through Mac-1/complement interaction, express ICAM-3 by themselves, and that LFA-1/ICAM-3 interaction might participate in the glomerular aggregation of leukocytes in MPGN type I. In this study, we could not conclude that LFA-1/ICAM-1 or Mac-1/ICAM-1 interaction was involved in the leukocyte accumulation in this disease.
KW - ICAM- 1
KW - ICAM-3
KW - LFA-1
KW - Mac-1
KW - Membranoproliferative glomerulonephritis type I
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U2 - 10.1016/S0272-6386(96)90249-8
DO - 10.1016/S0272-6386(96)90249-8
M3 - Article
C2 - 9158205
AN - SCOPUS:0029904962
VL - 28
SP - 685
EP - 694
JO - American Journal of Kidney Diseases
JF - American Journal of Kidney Diseases
SN - 0272-6386
IS - 5
ER -