Monocyte chemoattractant protein-1 mediates monocyte/macrophage influx in anti-thymocyte antibody-induced glomerulonephritis.
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Monocyte chemoattractant protein-1 mediates monocyte/macrophage influx in anti-thymocyte antibody-induced glomerulonephritis. / Wenzel, Ulrich; Schneider, A; Valente, A J; Abboud, H E; Thaiss, F; Helmchen, U M; Stahl, R A.
In: KIDNEY INT, Vol. 51, No. 3, 3, 1997, p. 770-776.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
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T1 - Monocyte chemoattractant protein-1 mediates monocyte/macrophage influx in anti-thymocyte antibody-induced glomerulonephritis.
AU - Wenzel, Ulrich
AU - Schneider, A
AU - Valente, A J
AU - Abboud, H E
AU - Thaiss, F
AU - Helmchen, U M
AU - Stahl, R A
PY - 1997
Y1 - 1997
N2 - Chemokines are a family of chemotactic cytokines whose participation in inflammation in vivo remains to be established. To study the role of monocyte-chemoattractant-protein-1 (MCP-1) on the glomerular accumulation of leukocytes, rats received a neutralizing anti-MCP-1 antiserum following the induction of an glomerulonephritis by an anti-thymocyte antibody (ATS). The infiltration of monocytes/macrophages (M/M) and granulocytes was analyzed by immunohistology. When studied by Northern blotting, glomerular mRNA levels of MCP-1, and interleukin 1 beta (IL-1 beta) increased at three hours and 24 hours following the induction of the injury. The glomerular mRNA expression of intercellular adhesion molecule-1 (ICAM-1) only increased marginally, whereas the expression of the chemokine RANTES was not enhanced. In animals that received anti-MCP-1 antibody glomerular MCP-1 mRNA expression increased. However, the chemoattractant activity for monocytes released into supernatants of isolated glomeruli was reduced. The anti-MCP-1 antibody did not affect glomerular IL-1 beta, ICAM-1 or RANTES mRNA levels. The induction of glomerulonephritis was associated with an increased glomerular recruitment of polymorphonuclear granulocytes (PMNs) at three hours and M/M at 24 hours, when compared with controls. The anti-MCP-1 antiserum significantly reduced the glomerular M/M infiltration at 24 hours by 40%, but was without effect on glomerular PMN recruitment or growth of the resident glomerular cells. These studies demonstrate that MCP-1 is an important mediator for monocyte recruitment in this model of glomerulonephritis. The reduction of M/M infiltration might affect this glomerular injury.
AB - Chemokines are a family of chemotactic cytokines whose participation in inflammation in vivo remains to be established. To study the role of monocyte-chemoattractant-protein-1 (MCP-1) on the glomerular accumulation of leukocytes, rats received a neutralizing anti-MCP-1 antiserum following the induction of an glomerulonephritis by an anti-thymocyte antibody (ATS). The infiltration of monocytes/macrophages (M/M) and granulocytes was analyzed by immunohistology. When studied by Northern blotting, glomerular mRNA levels of MCP-1, and interleukin 1 beta (IL-1 beta) increased at three hours and 24 hours following the induction of the injury. The glomerular mRNA expression of intercellular adhesion molecule-1 (ICAM-1) only increased marginally, whereas the expression of the chemokine RANTES was not enhanced. In animals that received anti-MCP-1 antibody glomerular MCP-1 mRNA expression increased. However, the chemoattractant activity for monocytes released into supernatants of isolated glomeruli was reduced. The anti-MCP-1 antibody did not affect glomerular IL-1 beta, ICAM-1 or RANTES mRNA levels. The induction of glomerulonephritis was associated with an increased glomerular recruitment of polymorphonuclear granulocytes (PMNs) at three hours and M/M at 24 hours, when compared with controls. The anti-MCP-1 antiserum significantly reduced the glomerular M/M infiltration at 24 hours by 40%, but was without effect on glomerular PMN recruitment or growth of the resident glomerular cells. These studies demonstrate that MCP-1 is an important mediator for monocyte recruitment in this model of glomerulonephritis. The reduction of M/M infiltration might affect this glomerular injury.
M3 - SCORING: Zeitschriftenaufsatz
VL - 51
SP - 770
EP - 776
JO - KIDNEY INT
JF - KIDNEY INT
SN - 0085-2538
IS - 3
M1 - 3
ER -