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Titolo:
Identification and kinetics of leukocytes after severe ischaemia/reperfusion renal injury
Autore:
Ysebaert, DK; De Greef, KE; Vercauteren, SR; Ghielli, M; Verpooten, GA; Eyskens, EJ; De Broe, ME;
Indirizzi:
Univ Antwerp, Dept Expt Surg, Antwerp, Belgium Univ Antwerp Antwerp Belgium Antwerp, Dept Expt Surg, Antwerp, Belgium Univ Antwerp, Dept Nephrol, Antwerp, Belgium Univ Antwerp Antwerp Belgium iv Antwerp, Dept Nephrol, Antwerp, Belgium
Titolo Testata:
NEPHROLOGY DIALYSIS TRANSPLANTATION
fascicolo: 10, volume: 15, anno: 2000,
pagine: 1562 - 1574
SICI:
0931-0509(200010)15:10<1562:IAKOLA>2.0.ZU;2-7
Fonte:
ISI
Lingua:
ENG
Soggetto:
REPERFUSION INJURY; RAT-KIDNEY; ISCHEMIA/REPERFUSION INJURY; MONOCLONAL-ANTIBODY; ADHESION-MOLECULES; FAILURE; NEUTROPHILS; ISCHEMIA; MACROPHAGES; INFLAMMATION;
Keywords:
damage; kidney; macrophages; myeloperoxidase; neutrophils; rat; regeneration;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
45
Recensione:
Indirizzi per estratti:
Indirizzo: De Broe, ME Univ Antwerp Hosp, Dept Nephrol Hypertens, Wilrijkstr 10, B-2650 Edegem, Belgium Univ Antwerp Hosp Wilrijkstr 10 Edegem Belgium B-2650 Belgium
Citazione:
D.K. Ysebaert et al., "Identification and kinetics of leukocytes after severe ischaemia/reperfusion renal injury", NEPH DIAL T, 15(10), 2000, pp. 1562-1574

Abstract

Background. Leukocyte adhesion/infiltration in response to renal ischaemia/reperfusion (I/R) injury is a well-known but poorly understood phenomenon The identification? kinetics, and exact role of these inflammatory cells inI/R injury and regeneration are still matters of debate. Methods. Uninephrectomized rats were submitted to 60 min renal ischaemia by clamping of renal vessels. Results. Seven acute renal failure was observed, with maximum functional impairment on day 2. By 12 h after the ischaemic event, up to 80% of proximal tubular cells in the outer stripe of outer medulla (OSOM) were already severely damaged. Proliferation (proliferating cell nuclear antigen (PCNA) staining) started after 24 h, reaching maximum activity on day 3. Regeneration of tubular morphology started on the 3rd day, and after 10 days 50% of tubules had regenerated completely. Interstitial leukocytes (OX-1 immunohistochemical staining) were already prominent at day 1, thereafter gradually increasing with time. The so-called neutrophil-specific identification methods (myeloperoxidase (MPO), chloroacetate esterase, mAb HIS48) proved to be non-specific, since they also stained for macrophages, as demonstrated by flow cytometry and the combination of these stainings with the macrophage-specific ED-1 staining, MPO activity was already significantly increased at 1 h post-I/R (439 +/- 34%, P < 0.005), reaching its maximum activity after 12h of I/R ( 1159 +/- 138%, P < 0.0005), declining thereafter. On the other hand, neutrophil presence investigated by H&E staining revealed only a few neutrophils in glomeruli, medullary rays, and OSOM at 24 h after the ischaemic event (4.7 +/- 4.2 cells/mm(2) vs controls = 2.3 +/- 2.0 cells/mm(2) (n.s.)), and remained unchanged over the next 10 days. In contrast, significant monocyte/macrophage adhesion/infiltration (ED-1 staining) occurred at the OSOM at 24 h post-ischaemia (at 24 h, 120 +/- 46 cells/mm(2) vs sham = 18+/- 4 cells/mm(2) (P < 0.05)), became prominent at day 5 (1034 +/- 161 cells/mm(2) vs sham = 18 +/- 18 cells/mm(2) (P< 0.05)), and almost disappearedafter 10 days. CD4(+) cells (W3/25) gradually increased from day 5, reaching a maximum at day 10. A few CD8(+) cells (OX-8) were apparent from days 3until 10, but no B-cells (OX-33) were observed. Conclusions. After severe warm I/R renal injury, a pronounced acute tubular necrosis occurs during the first 12-24 h in the absence of a marked cellular infiltrate, but with an important renal MPO activity, reflecting the activation of the adhering inflammatory cells (polymorphonuclear cells (PMNs)and mainly monocytes/macrophages). Only later at the time and site (OSOM) of regeneration a sequential accumulation of monocytes;macrophages and T cells becomes prominent, in contrast with the low number of neutrophils foundin the kidney during the 10-day post-ischaemic period. The non-specificityof the so-called neutrophil-specific identification methods (MPO activity,naphthol AS-D chloroacetate esterase, or mAb HIS-48 staining), cross-reacting with monocytes/macrophages, explains the controversy in literature concerning the number of PMNs in post-ischaemic injury.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 30/11/20 alle ore 07:03:05