Abstract
It was previously reported that the L-selectin ligands detected by a rat L-selectin and human IgG chimeric molecule (rLEC-IgG) are expressed in the distal tubules of the kidney, where no leukocyte traffic is seen under physiological conditions. In the present study, the role of L-selectin ligands in leukocyte infiltration into the kidney interstitium was investigated using a rat ureteric obstruction model. After ligation of the ureter, ligands for L-selectin rapidly disappeared from tubular epithelial cells and were relocated to the interstitium and peritubular capillary walls, where infiltration of monocytes and CD8+ T cells subsequently occurred. Mononuclear cell infiltration was significantly inhibited by intravenous injection of a neutralizing monoclonal antibody (MAb) against L-selectin, indicating the possible involvement of an L-selectin-mediated pathway. Interestingly, immunohistochemical studies with a MAb against sulphatide showed that the distribution of sulphatide, known to be one of the candidates of L-selectin ligand, was almost indistinguishable from the staining pattern of rLEC-IgG in both normal and ureteric obstructed kidneys, suggesting that sulphatide and/or related molecule(s) relocated to the renal interstitium were recognized by leukocyte L-selectin, leading to interstitial leukocyte infiltration. In line with this notion, intravenous injection of sulphatide markedly inhibited leukocyte infiltration, suggesting that L-selectin- sulphatide interaction may play a pivotal role in interstitial leukocyte infiltration in the kidney following ureteric obstruction.
| Original language | English |
|---|---|
| Pages (from-to) | 93-99 |
| Number of pages | 7 |
| Journal | Journal of Pathology |
| Volume | 188 |
| Issue number | 1 |
| DOIs | |
| Publication status | Published - 1999 |
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Keywords
- Inflammation
- L-selectin
- Obstructive nephropathy
- Sulphatide
ASJC Scopus subject areas
- Pathology and Forensic Medicine
Cite this
L-selectin and its ligands mediate infiltration of mononuclear cells into kidney interstitium after ureteric obstruction. / Shikata, Kenichi; Suzuki, Yasuo; Wada, Jun; Hirata, Kyoji; Matsuda, Mitsuhiro; Kawashima, Hiroto; Suzuki, Takashi; Iizuka, Masako; Makino, Hirofumi; Miyasaka, Masayuki.
In: Journal of Pathology, Vol. 188, No. 1, 1999, p. 93-99.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - L-selectin and its ligands mediate infiltration of mononuclear cells into kidney interstitium after ureteric obstruction
AU - Shikata, Kenichi
AU - Suzuki, Yasuo
AU - Wada, Jun
AU - Hirata, Kyoji
AU - Matsuda, Mitsuhiro
AU - Kawashima, Hiroto
AU - Suzuki, Takashi
AU - Iizuka, Masako
AU - Makino, Hirofumi
AU - Miyasaka, Masayuki
PY - 1999
Y1 - 1999
N2 - It was previously reported that the L-selectin ligands detected by a rat L-selectin and human IgG chimeric molecule (rLEC-IgG) are expressed in the distal tubules of the kidney, where no leukocyte traffic is seen under physiological conditions. In the present study, the role of L-selectin ligands in leukocyte infiltration into the kidney interstitium was investigated using a rat ureteric obstruction model. After ligation of the ureter, ligands for L-selectin rapidly disappeared from tubular epithelial cells and were relocated to the interstitium and peritubular capillary walls, where infiltration of monocytes and CD8+ T cells subsequently occurred. Mononuclear cell infiltration was significantly inhibited by intravenous injection of a neutralizing monoclonal antibody (MAb) against L-selectin, indicating the possible involvement of an L-selectin-mediated pathway. Interestingly, immunohistochemical studies with a MAb against sulphatide showed that the distribution of sulphatide, known to be one of the candidates of L-selectin ligand, was almost indistinguishable from the staining pattern of rLEC-IgG in both normal and ureteric obstructed kidneys, suggesting that sulphatide and/or related molecule(s) relocated to the renal interstitium were recognized by leukocyte L-selectin, leading to interstitial leukocyte infiltration. In line with this notion, intravenous injection of sulphatide markedly inhibited leukocyte infiltration, suggesting that L-selectin- sulphatide interaction may play a pivotal role in interstitial leukocyte infiltration in the kidney following ureteric obstruction.
AB - It was previously reported that the L-selectin ligands detected by a rat L-selectin and human IgG chimeric molecule (rLEC-IgG) are expressed in the distal tubules of the kidney, where no leukocyte traffic is seen under physiological conditions. In the present study, the role of L-selectin ligands in leukocyte infiltration into the kidney interstitium was investigated using a rat ureteric obstruction model. After ligation of the ureter, ligands for L-selectin rapidly disappeared from tubular epithelial cells and were relocated to the interstitium and peritubular capillary walls, where infiltration of monocytes and CD8+ T cells subsequently occurred. Mononuclear cell infiltration was significantly inhibited by intravenous injection of a neutralizing monoclonal antibody (MAb) against L-selectin, indicating the possible involvement of an L-selectin-mediated pathway. Interestingly, immunohistochemical studies with a MAb against sulphatide showed that the distribution of sulphatide, known to be one of the candidates of L-selectin ligand, was almost indistinguishable from the staining pattern of rLEC-IgG in both normal and ureteric obstructed kidneys, suggesting that sulphatide and/or related molecule(s) relocated to the renal interstitium were recognized by leukocyte L-selectin, leading to interstitial leukocyte infiltration. In line with this notion, intravenous injection of sulphatide markedly inhibited leukocyte infiltration, suggesting that L-selectin- sulphatide interaction may play a pivotal role in interstitial leukocyte infiltration in the kidney following ureteric obstruction.
KW - Inflammation
KW - L-selectin
KW - Obstructive nephropathy
KW - Sulphatide
UR - http://www.scopus.com/inward/record.url?scp=0032916847&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0032916847&partnerID=8YFLogxK
U2 - 10.1002/(SICI)1096-9896(199905)188:1<93::AID-PATH305>3.0.CO;2-#
DO - 10.1002/(SICI)1096-9896(199905)188:1<93::AID-PATH305>3.0.CO;2-#
M3 - Article
C2 - 10398147
AN - SCOPUS:0032916847
VL - 188
SP - 93
EP - 99
JO - Journal of Pathology
JF - Journal of Pathology
SN - 0022-3417
IS - 1
ER -