scholarly journals The blocking of CXCR3 and CCR5 suppresses the infiltration of T lymphocytes in rat renal ischemia reperfusion

2012 ◽  
Vol 27 (10) ◽  
pp. 3799-3806 ◽  
Author(s):  
K. Tsutahara ◽  
M. Okumi ◽  
Y. Kakuta ◽  
T. Abe ◽  
K. Yazawa ◽  
...  
Keyword(s):  
T Lymphocytes ◽  
Ischemia Reperfusion ◽  
Renal Ischemia

Abstract P332: Role of T-Lymphocytes in the Long-Term Blood Pressure and Renal Disease Effects of Acute Renal Ischemia-Reperfusion Injury

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Bernardo Lopez ◽  
Galina Petrova ◽  
Justine M Abais-Battad ◽  
Hayley Lund ◽  
Daniel Fehrenbach ◽  
...  
Keyword(s):  
T Cells ◽  
T Lymphocytes ◽  
Renal Damage ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Immunosuppressive Agents ◽  
High Salt ◽  
Renal Ischemia ◽  
Salt Sensitive Hypertension

Epidemiological data indicates that acute kidney injury (AKI) is an independent risk factor for the development of hypertension and chronic kidney disease in patients. Previous studies demonstrated that rats develop sodium-dependent hypertension and kidney damage following experimental AKI induced by a renal ischemia-reperfusion (IR) insult; furthermore, these high salt deleterious effects could be blunted by administration of immunosuppressive agents. The present study was performed on Dahl SS (SS) rats and SS rats with a null mutation in the CD247 gene (SS-CD247) leading to depletion of T-lymphocytes in order to specifically examine the role of T cells in this response (n=5-6 rats/group). As assessed by serum creatinine (SCr) levels, no difference was observed in the initial response to IR injury between SS and SS-CD247: SCr increased from 0.44±0.03 to 2.16±0.32 mg/dl in SS rats 24 hours after an initial 30 minute period of renal ischemia and returned to control levels after 8 days of recovery. Moreover, no differences were noted in mean arterial pressure (MAP) or albumin excretion rate (UAlb) between SS and SS-CD247 after 43 days of recovery from IR injury while the rats were maintained on a low salt (0.4% NaCl) diet. When the rats were fed a 4.0% NaCl diet for two weeks, MAP and UAlb significantly increased in the sham SS to 178±9 mmHg and 189±25 mg/day, respectively; values significantly greater than observed in the sham SS-CD247 rats (148±2 mmHg and 87±17 mg/day). As expected, the SS rats recovered from IR injury demonstrated an exaggerated increase in MAP (peaking at 183±2 mmHg) and UAlb (275±54 mg/day) in response to high salt. There was no difference in the number of total CD3+ lymphocytes in the kidneys of IR and sham SS after high salt, though the ratio of CD4+/CD8+ T cells was increased in the IR group. Compared to sham CD247, an exaggerated elevation of MAP (157±9 mmHg) and UAlb (210±32 mg/day) was also observed in the SS-CD247 rats recovered from IR injury, demonstrating enhanced responsiveness following IR injury in animals lacking T cells. These data indicate that T lymphocytes amplify salt-sensitive hypertension and renal damage, but other mechanisms also mediate the salt-sensitive hypertension and renal damage that occurs in animals recovered from IR injury.

scholarly journals Renal ischemia-reperfusion leads to long term infiltration of activated and effector-memory T lymphocytes

2009 ◽  
Vol 75 (5) ◽  
pp. 526-535 ◽  
Author(s):  
Miguel Ascon ◽  
Dolores B. Ascon ◽  
Manchang Liu ◽  
Chris Cheadle ◽  
Chaitali Sarkar ◽  
...  
Keyword(s):  
T Lymphocytes ◽  
Ischemia Reperfusion ◽  
Renal Ischemia ◽  
Effector Memory ◽  
Memory T Lymphocytes

The Blocking of CXCR3 and CCR5 Suppresses the Infiltration of T Lymphocytes in Rat Renal Ischemia Reperfusion

2012 ◽  
Vol 94 (10S) ◽  
pp. 1138
Author(s):  
K. Tsutahara ◽  
M. Okumi ◽  
Y. Kakuta ◽  
T. Kato ◽  
T. Abe ◽  
...  
Keyword(s):  
T Lymphocytes ◽  
Ischemia Reperfusion ◽  
Renal Ischemia

Contribution of T lymphocytes to rat renal ischemia/reperfusion injury

2009 ◽  
Vol 13 (1) ◽  
pp. 25-32 ◽  
Author(s):  
Eisei Noiri ◽  
Kent Doi ◽  
Reiko Inagi ◽  
Masaomi Nangaku ◽  
Toshiro Fujita
Keyword(s):  
T Lymphocytes ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Renal Ischemia ◽  
Renal Ischemia Reperfusion Injury

Injury in renal ischemia-reperfusion is independent from immunoglobulins and T lymphocytes

2002 ◽  
Vol 282 (2) ◽  
pp. F352-F357 ◽  
Author(s):  
Pierce Park ◽  
Mark Haas ◽  
Patrick N. Cunningham ◽  
Lihua Bao ◽  
Jessy J. Alexander ◽  
...  
Keyword(s):  
T Lymphocytes ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Renal Ischemia ◽  
Nitrogen Levels ◽  
Tubular Necrosis ◽  
Organ Systems ◽  
Recombination Activating Gene ◽  
Rag 1 ◽  
Natural Igm

Ischemia-reperfusion injury (IRI) is a complex and incompletely understood process involving a cascade of events that culminates in apoptotic and/or necrotic cell death. Natural IgM antibodies and complement have been implicated in the pathogenesis of IRI in a variety of organ systems as have T lymphocytes in renal IRI. To investigate the role of Ig and T lymphocytes in renal IRI, recombination-activating gene (RAG)-1-deficient mice were studied. RAG-1(−/−) mice were not protected from acute renal failure induced by 27.5 min of bilateral renal ischemia and subsequent reperfusion [serum urea nitrogen levels 30 h after reperfusion, 155.2 ± 5.6 and 152.8 ± 11.4 mg/dl in RAG-1(−/−) and wild-type mice, respectively; n = 13 each]. Histological examination showed acute tubular necrosis and neutrophilic infiltration with no significant differences between groups. In contrast with other organ systems, Igs were not found in kidneys at time points ranging from 1 min to 30 h after ischemia. Thus Igs and mature T lymphocytes do not appear to play a significant role in the pathogenesis of IRI in the kidney.

1843: Role of Cxcr2 in Renal Ischemia/Reperfusion Injury

2004 ◽  
Vol 171 (4S) ◽  
pp. 487-487
Author(s):  
Motoo Araki ◽  
Masayoshi Miura ◽  
Hiromi Kumon ◽  
John Belperio ◽  
Robert Strieter ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Renal Ischemia ◽  
Renal Ischemia Reperfusion Injury
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