Peritoneal Dialysis Aggravates and Accelerates Atherosclerosis in Uremic ApoE −/− Mice
Atherosclerosis is highly prevalent in people with chronic kidney disease (CKD), including those receiving peritoneal dialysis (PD). Although it is lifesaving, PD induces profound systemic inflammation, which may aggravate atherosclerosis. Therefore, the hypothesis is that this PD-induced inflammati...
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| Vydáno v: | Journal of the American Heart Association Ročník 13; číslo 14; s. e034066 |
|---|---|
| Hlavní autoři: | , , , , , , , , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | angličtina |
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England
John Wiley and Sons Inc
16.07.2024
Wiley |
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| ISSN: | 2047-9980, 2047-9980 |
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| Abstract | Atherosclerosis is highly prevalent in people with chronic kidney disease (CKD), including those receiving peritoneal dialysis (PD). Although it is lifesaving, PD induces profound systemic inflammation, which may aggravate atherosclerosis. Therefore, the hypothesis is that this PD-induced inflammation aggravates atherosclerosis via immune cell activation.
mice were subjected to a 5/6 nephrectomy to induce CKD. Three weeks later, mice were fed a high-cholesterol diet. Half of the nephrectomized mice then received daily peritoneal infusions of 3.86% Physioneal for 67 further days (CKD+PD) until the end of the experiment, and were compared with mice without CKD. Sham operated and PD-only mice were additional controls. CKD+PD mice displayed more severe atherosclerotic disease than control mice. Plaque area increased, and plaques were more advanced with a vulnerable phenotype typified by decreased collagen content and decreased fibrous cap thickness. Increased CD3
T-cell numbers were present in plaques and perivascular adipose tissue of CKD and CKD+PD mice. Plaques of CKD+PD mice contained more iNOS
immune cells. Spleens of CKD+PD mice showed more CD4
central memory, terminally differentiated type 1 T-helper (Th1), Th17, and CX3C motif chemokine receptor 1
(CX3CR1) CD4
T-cells with less regulatory and effector T-cells.
PD-fluid exposure in uremic mice potentiates systemic and vascular T-cell-driven inflammation and aggravates atherosclerosis. PD polarized CD4
T-cells toward an inflammatory Th1/Th17 phenotype, and increased CX3CR1
CD4
T-cells, which are associated with vascular homing in CKD-associated atherosclerosis. Targeting CD4
T-cell activation and CX3CR1
polarization has the potential to attenuate atherosclerosis in PD patients. |
|---|---|
| AbstractList | Background Atherosclerosis is highly prevalent in people with chronic kidney disease (CKD), including those receiving peritoneal dialysis (PD). Although it is lifesaving, PD induces profound systemic inflammation, which may aggravate atherosclerosis. Therefore, the hypothesis is that this PD‐induced inflammation aggravates atherosclerosis via immune cell activation. Methods and Results ApoE−/− mice were subjected to a 5/6 nephrectomy to induce CKD. Three weeks later, mice were fed a high‐cholesterol diet. Half of the nephrectomized mice then received daily peritoneal infusions of 3.86% Physioneal for 67 further days (CKD+PD) until the end of the experiment, and were compared with mice without CKD. Sham operated and PD‐only mice were additional controls. CKD+PD mice displayed more severe atherosclerotic disease than control mice. Plaque area increased, and plaques were more advanced with a vulnerable phenotype typified by decreased collagen content and decreased fibrous cap thickness. Increased CD3+ T‐cell numbers were present in plaques and perivascular adipose tissue of CKD and CKD+PD mice. Plaques of CKD+PD mice contained more iNOS+ immune cells. Spleens of CKD+PD mice showed more CD4+ central memory, terminally differentiated type 1 T‐helper (Th1), Th17, and CX3C motif chemokine receptor 1+ (CX3CR1) CD4+ T‐cells with less regulatory and effector T‐cells. Conclusions PD‐fluid exposure in uremic mice potentiates systemic and vascular T‐cell‐driven inflammation and aggravates atherosclerosis. PD polarized CD4+ T‐cells toward an inflammatory Th1/Th17 phenotype, and increased CX3CR1+ CD4+ T‐cells, which are associated with vascular homing in CKD‐associated atherosclerosis. Targeting CD4+ T‐cell activation and CX3CR1+ polarization has the potential to attenuate atherosclerosis in PD patients. Atherosclerosis is highly prevalent in people with chronic kidney disease (CKD), including those receiving peritoneal dialysis (PD). Although it is lifesaving, PD induces profound systemic inflammation, which may aggravate atherosclerosis. Therefore, the hypothesis is that this PD-induced inflammation aggravates atherosclerosis via immune cell activation.BACKGROUNDAtherosclerosis is highly prevalent in people with chronic kidney disease (CKD), including those receiving peritoneal dialysis (PD). Although it is lifesaving, PD induces profound systemic inflammation, which may aggravate atherosclerosis. Therefore, the hypothesis is that this PD-induced inflammation aggravates atherosclerosis via immune cell activation.ApoE-/- mice were subjected to a 5/6 nephrectomy to induce CKD. Three weeks later, mice were fed a high-cholesterol diet. Half of the nephrectomized mice then received daily peritoneal infusions of 3.86% Physioneal for 67 further days (CKD+PD) until the end of the experiment, and were compared with mice without CKD. Sham operated and PD-only mice were additional controls. CKD+PD mice displayed more severe atherosclerotic disease than control mice. Plaque area increased, and plaques were more advanced with a vulnerable phenotype typified by decreased collagen content and decreased fibrous cap thickness. Increased CD3+ T-cell numbers were present in plaques and perivascular adipose tissue of CKD and CKD+PD mice. Plaques of CKD+PD mice contained more iNOS+ immune cells. Spleens of CKD+PD mice showed more CD4+ central memory, terminally differentiated type 1 T-helper (Th1), Th17, and CX3C motif chemokine receptor 1+ (CX3CR1) CD4+ T-cells with less regulatory and effector T-cells.METHODS AND RESULTSApoE-/- mice were subjected to a 5/6 nephrectomy to induce CKD. Three weeks later, mice were fed a high-cholesterol diet. Half of the nephrectomized mice then received daily peritoneal infusions of 3.86% Physioneal for 67 further days (CKD+PD) until the end of the experiment, and were compared with mice without CKD. Sham operated and PD-only mice were additional controls. CKD+PD mice displayed more severe atherosclerotic disease than control mice. Plaque area increased, and plaques were more advanced with a vulnerable phenotype typified by decreased collagen content and decreased fibrous cap thickness. Increased CD3+ T-cell numbers were present in plaques and perivascular adipose tissue of CKD and CKD+PD mice. Plaques of CKD+PD mice contained more iNOS+ immune cells. Spleens of CKD+PD mice showed more CD4+ central memory, terminally differentiated type 1 T-helper (Th1), Th17, and CX3C motif chemokine receptor 1+ (CX3CR1) CD4+ T-cells with less regulatory and effector T-cells.PD-fluid exposure in uremic mice potentiates systemic and vascular T-cell-driven inflammation and aggravates atherosclerosis. PD polarized CD4+ T-cells toward an inflammatory Th1/Th17 phenotype, and increased CX3CR1+ CD4+ T-cells, which are associated with vascular homing in CKD-associated atherosclerosis. Targeting CD4+ T-cell activation and CX3CR1+ polarization has the potential to attenuate atherosclerosis in PD patients.CONCLUSIONSPD-fluid exposure in uremic mice potentiates systemic and vascular T-cell-driven inflammation and aggravates atherosclerosis. PD polarized CD4+ T-cells toward an inflammatory Th1/Th17 phenotype, and increased CX3CR1+ CD4+ T-cells, which are associated with vascular homing in CKD-associated atherosclerosis. Targeting CD4+ T-cell activation and CX3CR1+ polarization has the potential to attenuate atherosclerosis in PD patients. Atherosclerosis is highly prevalent in people with chronic kidney disease (CKD), including those receiving peritoneal dialysis (PD). Although it is lifesaving, PD induces profound systemic inflammation, which may aggravate atherosclerosis. Therefore, the hypothesis is that this PD-induced inflammation aggravates atherosclerosis via immune cell activation. mice were subjected to a 5/6 nephrectomy to induce CKD. Three weeks later, mice were fed a high-cholesterol diet. Half of the nephrectomized mice then received daily peritoneal infusions of 3.86% Physioneal for 67 further days (CKD+PD) until the end of the experiment, and were compared with mice without CKD. Sham operated and PD-only mice were additional controls. CKD+PD mice displayed more severe atherosclerotic disease than control mice. Plaque area increased, and plaques were more advanced with a vulnerable phenotype typified by decreased collagen content and decreased fibrous cap thickness. Increased CD3 T-cell numbers were present in plaques and perivascular adipose tissue of CKD and CKD+PD mice. Plaques of CKD+PD mice contained more iNOS immune cells. Spleens of CKD+PD mice showed more CD4 central memory, terminally differentiated type 1 T-helper (Th1), Th17, and CX3C motif chemokine receptor 1 (CX3CR1) CD4 T-cells with less regulatory and effector T-cells. PD-fluid exposure in uremic mice potentiates systemic and vascular T-cell-driven inflammation and aggravates atherosclerosis. PD polarized CD4 T-cells toward an inflammatory Th1/Th17 phenotype, and increased CX3CR1 CD4 T-cells, which are associated with vascular homing in CKD-associated atherosclerosis. Targeting CD4 T-cell activation and CX3CR1 polarization has the potential to attenuate atherosclerosis in PD patients. |
| Author | Hoeksema‐Hackmann, Sanne Grefhorst, Aldo Bosmans, Laura A. den Toom, Myrthe Beckers, Linda Kane, Jamie Eringa, Etto C. van Os, Bram W. Gijbels, Marion J. Lutgens, Esther Moen‐de Wit, Denise Vervloet, Marc G. Jakulj, Lily Vos, Winnie G. Levels, Johannes H. M. |
| AuthorAffiliation | 5 Animal Research Institute AMC Amsterdam University Medical Centre Amsterdam the Netherlands 3 Department of Medical Biochemistry, Amsterdam Cardiovascular Sciences, Amsterdam Immunity and Infection Amsterdam University Medical Centre Amsterdam the Netherlands 8 Department of Nephrology Radboud University Medical Centre Nijmegen the Netherlands 1 Department of Nephrology, Amsterdam Cardiovascular Sciences Amsterdam University Medical Centre Amsterdam the Netherlands 10 Department of Physiology Maastricht University Maastricht the Netherlands 2 Department of Physiology, Amsterdam Cardiovascular Sciences Amsterdam University Medical Centre Amsterdam the Netherlands 6 Department of Pathology, Cardiovascular Research Institute Maastricht (CARIM) Maastricht University Medical Centre Maastricht the Netherlands 4 Department of Experimental Vascular Medicine, Amsterdam Cardiovascular Sciences Amsterdam University Medical Centre Amsterdam the Netherlands 7 Dianet Dialysis Centre Amsterdam Amsterdam th |
| AuthorAffiliation_xml | – name: 6 Department of Pathology, Cardiovascular Research Institute Maastricht (CARIM) Maastricht University Medical Centre Maastricht the Netherlands – name: 4 Department of Experimental Vascular Medicine, Amsterdam Cardiovascular Sciences Amsterdam University Medical Centre Amsterdam the Netherlands – name: 1 Department of Nephrology, Amsterdam Cardiovascular Sciences Amsterdam University Medical Centre Amsterdam the Netherlands – name: 9 Department of Cardiovascular Medicine and Immunology Mayo Clinic Rochester MN – name: 5 Animal Research Institute AMC Amsterdam University Medical Centre Amsterdam the Netherlands – name: 2 Department of Physiology, Amsterdam Cardiovascular Sciences Amsterdam University Medical Centre Amsterdam the Netherlands – name: 7 Dianet Dialysis Centre Amsterdam Amsterdam the Netherlands – name: 3 Department of Medical Biochemistry, Amsterdam Cardiovascular Sciences, Amsterdam Immunity and Infection Amsterdam University Medical Centre Amsterdam the Netherlands – name: 8 Department of Nephrology Radboud University Medical Centre Nijmegen the Netherlands – name: 10 Department of Physiology Maastricht University Maastricht the Netherlands |
| Author_xml | – sequence: 1 givenname: Jamie orcidid: 0009-0005-0129-0075 surname: Kane fullname: Kane, Jamie – sequence: 2 givenname: Winnie G. orcidid: 0000-0001-7805-7275 surname: Vos fullname: Vos, Winnie G. – sequence: 3 givenname: Laura A. orcidid: 0000-0002-1984-9691 surname: Bosmans fullname: Bosmans, Laura A. – sequence: 4 givenname: Bram W. surname: van Os fullname: van Os, Bram W. – sequence: 5 givenname: Myrthe surname: den Toom fullname: den Toom, Myrthe – sequence: 6 givenname: Sanne surname: Hoeksema‐Hackmann fullname: Hoeksema‐Hackmann, Sanne – sequence: 7 givenname: Denise surname: Moen‐de Wit fullname: Moen‐de Wit, Denise – sequence: 8 givenname: Marion J. orcidid: 0000-0002-4906-0384 surname: Gijbels fullname: Gijbels, Marion J. – sequence: 9 givenname: Linda surname: Beckers fullname: Beckers, Linda – sequence: 10 givenname: Aldo orcidid: 0000-0003-1761-9494 surname: Grefhorst fullname: Grefhorst, Aldo – sequence: 11 givenname: Johannes H. M. orcidid: 0000-0002-8946-8819 surname: Levels fullname: Levels, Johannes H. M. – sequence: 12 givenname: Lily orcidid: 0000-0002-8678-682X surname: Jakulj fullname: Jakulj, Lily – sequence: 13 givenname: Marc G. orcidid: 0000-0003-4607-9415 surname: Vervloet fullname: Vervloet, Marc G. – sequence: 14 givenname: Esther orcidid: 0000-0002-2609-5744 surname: Lutgens fullname: Lutgens, Esther – sequence: 15 givenname: Etto C. orcidid: 0000-0002-9814-5149 surname: Eringa fullname: Eringa, Etto C. |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/38979792$$D View this record in MEDLINE/PubMed |
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| Copyright | 2024 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley. |
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| Issue | 14 |
| Keywords | atherosclerosis chronic kidney disease peritoneal dialysis inflammation kidney replacement therapy |
| Language | English |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 This manuscript was sent to Julie K. Freed, MD, PhD, Associate Editor, for review by expert referees, editorial decision, and final disposition. E. Lutgens and E. C. Eringa contributed equally. Supplemental Material is available at https://www.ahajournals.org/doi/suppl/10.1161/JAHA.123.034066 For Sources of Funding and Disclosures, see page 13. |
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| Snippet | Atherosclerosis is highly prevalent in people with chronic kidney disease (CKD), including those receiving peritoneal dialysis (PD). Although it is lifesaving,... Background Atherosclerosis is highly prevalent in people with chronic kidney disease (CKD), including those receiving peritoneal dialysis (PD). Although it is... |
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| SubjectTerms | atherosclerosis chronic kidney disease inflammation kidney replacement therapy Original Research peritoneal dialysis |
| Title | Peritoneal Dialysis Aggravates and Accelerates Atherosclerosis in Uremic ApoE −/− Mice |
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