Effects of Spermidine and p-Cresol on Polymorphonuclear Cell Apoptosis and Function
Polymorphonuclear leukocytes (PMNs) from chronic kidney disease (CKD) patients display accelerated apoptosis and dysfunction, which may predispose CKD patients to infections. In this study, we investigated the effect of spermidine and p‐cresol on apoptosis and function on PMN from healthy subjects....
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Published in | Artificial organs Vol. 35; no. 2; pp. E27 - E32 |
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Main Authors | , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Malden, USA
Blackwell Publishing Inc
01.02.2011
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Subjects | |
Online Access | Get full text |
ISSN | 0160-564X 1525-1594 1525-1594 |
DOI | 10.1111/j.1525-1594.2010.01116.x |
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Abstract | Polymorphonuclear leukocytes (PMNs) from chronic kidney disease (CKD) patients display accelerated apoptosis and dysfunction, which may predispose CKD patients to infections. In this study, we investigated the effect of spermidine and p‐cresol on apoptosis and function on PMN from healthy subjects. We measured the effect of spermidine and p‐cresol on apoptosis, ROS production unstimulated and stimulated (S. aureus and PMA) and expression of CD95, caspase 3, and CD11b on PMN. After incubation with p‐cresol and spermidine, we did not observe any changes in apoptosis, viability or expression of caspase 3 and CD95 in PMN from healthy subjects. PMN incubated for 10 minutes with spermidine demonstrated a significant reduction in spontaneous, S. aureus and PMA‐stimulated ROS production. p‐cresol induced a decrease in PMA‐stimulated ROS production. Spermidine and p‐cresol also induced a decrease in the expression of CD11b on PMN. Spermidine and p‐cresol decreased the expression of CD11b and oxidative burst of PMN from healthy subjects and had no effect on PMN apoptosis and viability. |
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AbstractList | Polymorphonuclear leukocytes (PMNs) from chronic kidney disease (CKD) patients display accelerated apoptosis and dysfunction, which may predispose CKD patients to infections. In this study, we investigated the effect of spermidine and p-cresol on apoptosis and function on PMN from healthy subjects. We measured the effect of spermidine and p-cresol on apoptosis, ROS production unstimulated and stimulated (S. aureus and PMA) and expression of CD95, caspase 3, and CD11b on PMN. After incubation with p-cresol and spermidine, we did not observe any changes in apoptosis, viability or expression of caspase 3 and CD95 in PMN from healthy subjects. PMN incubated for 10 minutes with spermidine demonstrated a significant reduction in spontaneous, S. aureus and PMA-stimulated ROS production. p-cresol induced a decrease in PMA-stimulated ROS production. Spermidine and p-cresol also induced a decrease in the expression of CD11b on PMN. Spermidine and p-cresol decreased the expression of CD11b and oxidative burst of PMN from healthy subjects and had no effect on PMN apoptosis and viability. Polymorphonuclear leukocytes (PMNs) from chronic kidney disease (CKD) patients display accelerated apoptosis and dysfunction, which may predispose CKD patients to infections. In this study, we investigated the effect of spermidine and p‐cresol on apoptosis and function on PMN from healthy subjects. We measured the effect of spermidine and p‐cresol on apoptosis, ROS production unstimulated and stimulated ( S. aureus and PMA) and expression of CD95, caspase 3, and CD11b on PMN. After incubation with p‐cresol and spermidine, we did not observe any changes in apoptosis, viability or expression of caspase 3 and CD95 in PMN from healthy subjects. PMN incubated for 10 minutes with spermidine demonstrated a significant reduction in spontaneous, S. aureus and PMA‐stimulated ROS production. p‐cresol induced a decrease in PMA‐stimulated ROS production. Spermidine and p‐cresol also induced a decrease in the expression of CD11b on PMN. Spermidine and p‐cresol decreased the expression of CD11b and oxidative burst of PMN from healthy subjects and had no effect on PMN apoptosis and viability. Polymorphonuclear leukocytes (PMNs) from chronic kidney disease (CKD) patients display accelerated apoptosis and dysfunction, which may predispose CKD patients to infections. In this study, we investigated the effect of spermidine and p-cresol on apoptosis and function on PMN from healthy subjects. We measured the effect of spermidine and p-cresol on apoptosis, ROS production unstimulated and stimulated (S. aureus and PMA) and expression of CD95, caspase 3, and CD11b on PMN. After incubation with p-cresol and spermidine, we did not observe any changes in apoptosis, viability or expression of caspase 3 and CD95 in PMN from healthy subjects. PMN incubated for 10 minutes with spermidine demonstrated a significant reduction in spontaneous, S. aureus and PMA-stimulated ROS production. p-cresol induced a decrease in PMA-stimulated ROS production. Spermidine and p-cresol also induced a decrease in the expression of CD11b on PMN. Spermidine and p-cresol decreased the expression of CD11b and oxidative burst of PMN from healthy subjects and had no effect on PMN apoptosis and viability.Polymorphonuclear leukocytes (PMNs) from chronic kidney disease (CKD) patients display accelerated apoptosis and dysfunction, which may predispose CKD patients to infections. In this study, we investigated the effect of spermidine and p-cresol on apoptosis and function on PMN from healthy subjects. We measured the effect of spermidine and p-cresol on apoptosis, ROS production unstimulated and stimulated (S. aureus and PMA) and expression of CD95, caspase 3, and CD11b on PMN. After incubation with p-cresol and spermidine, we did not observe any changes in apoptosis, viability or expression of caspase 3 and CD95 in PMN from healthy subjects. PMN incubated for 10 minutes with spermidine demonstrated a significant reduction in spontaneous, S. aureus and PMA-stimulated ROS production. p-cresol induced a decrease in PMA-stimulated ROS production. Spermidine and p-cresol also induced a decrease in the expression of CD11b on PMN. Spermidine and p-cresol decreased the expression of CD11b and oxidative burst of PMN from healthy subjects and had no effect on PMN apoptosis and viability. |
Author | Manfredi, Silvia R. Peres, Alines T. de Carvalho Jr, Jose Tarcisio G. Guimarães-Souza, Nadia Cendoroglo, Miguel Goes, Miguel A. Dalboni, Maria A. Watanabe, Renato Canziani, Maria E. Cendoroglo, Gabriel S. Batista, Marcelo C. |
Author_xml | – sequence: 1 givenname: Jose Tarcisio G. surname: de Carvalho Jr fullname: de Carvalho Jr, Jose Tarcisio G. organization: Department of Internal Medicine, Division of Nephrology, Federal University of São Paulo, São Paulo, Brazil; and – sequence: 2 givenname: Maria A. surname: Dalboni fullname: Dalboni, Maria A. organization: Department of Internal Medicine, Division of Nephrology, Federal University of São Paulo, São Paulo, Brazil; and – sequence: 3 givenname: Renato surname: Watanabe fullname: Watanabe, Renato organization: Department of Internal Medicine, Division of Nephrology, Federal University of São Paulo, São Paulo, Brazil; and – sequence: 4 givenname: Alines T. surname: Peres fullname: Peres, Alines T. organization: Department of Internal Medicine, Division of Nephrology, Federal University of São Paulo, São Paulo, Brazil; and – sequence: 5 givenname: Miguel A. surname: Goes fullname: Goes, Miguel A. organization: Department of Internal Medicine, Division of Nephrology, Federal University of São Paulo, São Paulo, Brazil; and – sequence: 6 givenname: Silvia R. surname: Manfredi fullname: Manfredi, Silvia R. organization: Department of Internal Medicine, Division of Nephrology, Federal University of São Paulo, São Paulo, Brazil; and – sequence: 7 givenname: Maria E. surname: Canziani fullname: Canziani, Maria E. organization: Department of Internal Medicine, Division of Nephrology, Federal University of São Paulo, São Paulo, Brazil; and – sequence: 8 givenname: Gabriel S. surname: Cendoroglo fullname: Cendoroglo, Gabriel S. organization: Department of Internal Medicine, Division of Nephrology, Federal University of São Paulo, São Paulo, Brazil; and – sequence: 9 givenname: Nadia surname: Guimarães-Souza fullname: Guimarães-Souza, Nadia organization: Department of Internal Medicine, Division of Nephrology, Federal University of São Paulo, São Paulo, Brazil; and – sequence: 10 givenname: Marcelo C. surname: Batista fullname: Batista, Marcelo C. organization: Department of Internal Medicine, Division of Nephrology, Federal University of São Paulo, São Paulo, Brazil; and – sequence: 11 givenname: Miguel surname: Cendoroglo fullname: Cendoroglo, Miguel organization: Department of Internal Medicine, Division of Nephrology, Federal University of São Paulo, São Paulo, Brazil; and |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/21314835$$D View this record in MEDLINE/PubMed |
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CitedBy_id | crossref_primary_10_1111_j_1525_1594_2012_01438_x crossref_primary_10_1053_j_jrn_2014_10_010 crossref_primary_10_1016_j_toxlet_2019_03_002 crossref_primary_10_3892_br_2025_1958 |
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SubjectTerms | Apoptosis Apoptosis - drug effects CD11b Antigen - immunology Cresols - pharmacology Humans Immune dysfunction Neutrophils - cytology Neutrophils - drug effects Neutrophils - immunology Neutrophils - metabolism Reactive Oxygen Species - metabolism Reactive oxygen species production Spermidine - pharmacology Uremic toxins |
Title | Effects of Spermidine and p-Cresol on Polymorphonuclear Cell Apoptosis and Function |
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