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CC‐chemokine receptor 7 (CCR7) deficiency alters adipose tissue leukocyte populations in mice
The mechanism by which macrophages and other immune cells accumulate in adipose tissue (AT) has been an area of intense investigation over the past decade. Several different chemokines and their cognate receptors have been studied for their role as chemoattractants in promoting recruitment of immune...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5037919/ https://www.ncbi.nlm.nih.gov/pubmed/27655794 http://dx.doi.org/10.14814/phy2.12971 |
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author | Orr, Jeb S. Kennedy, Arion J. Hill, Andrea A. Anderson‐Baucum, Emily K. Hubler, Merla J. Hasty, Alyssa H. |
author_facet | Orr, Jeb S. Kennedy, Arion J. Hill, Andrea A. Anderson‐Baucum, Emily K. Hubler, Merla J. Hasty, Alyssa H. |
author_sort | Orr, Jeb S. |
collection | PubMed |
description | The mechanism by which macrophages and other immune cells accumulate in adipose tissue (AT) has been an area of intense investigation over the past decade. Several different chemokines and their cognate receptors have been studied for their role as chemoattractants in promoting recruitment of immune cells to AT. However, it is also possible that chemoattractants known to promote clearance of immune cells from tissues to regional lymph nodes might be a critical component to overall AT immune homeostasis. In this study, we evaluated whether CCR7 influences AT macrophage (ATM) or T‐cell (ATT) accumulation. CCR7(−/−) and littermate wild‐type (WT) mice were placed on low‐fat diet (LFD) or high‐fat diet (HFD) for 16 weeks. CCR7 deficiency did not impact HFD‐induced weight gain, hepatic steatosis, or glucose intolerance. Although lean CCR7(−/−) mice had an increased proportion of alternatively activated ATMs, there were no differences in ATM accumulation or polarization between HFD‐fed CCR7(−/−) mice and their WT counterparts. However, CCR7 deficiency did lead to the preferential accumulation of CD8(+) ATT cells, which was further exacerbated by HFD feeding. Finally, expression of inflammatory cytokines/chemokines, such as Tnf, Il6, Il1β, Ccl2, and Ccl3, was equally elevated in AT by HFD feeding in CCR7(−/−) and WT mice, while Ifng and Il18 were elevated by HFD feeding in CCR7(−/−) but not in WT mice. Together, these data suggest that CCR7 plays a role in CD8(+) ATT cell egress, but does not influence ATM accumulation or the metabolic impact of diet‐induced obesity. |
format | Online Article Text |
id | pubmed-5037919 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-50379192016-09-30 CC‐chemokine receptor 7 (CCR7) deficiency alters adipose tissue leukocyte populations in mice Orr, Jeb S. Kennedy, Arion J. Hill, Andrea A. Anderson‐Baucum, Emily K. Hubler, Merla J. Hasty, Alyssa H. Physiol Rep Original Research The mechanism by which macrophages and other immune cells accumulate in adipose tissue (AT) has been an area of intense investigation over the past decade. Several different chemokines and their cognate receptors have been studied for their role as chemoattractants in promoting recruitment of immune cells to AT. However, it is also possible that chemoattractants known to promote clearance of immune cells from tissues to regional lymph nodes might be a critical component to overall AT immune homeostasis. In this study, we evaluated whether CCR7 influences AT macrophage (ATM) or T‐cell (ATT) accumulation. CCR7(−/−) and littermate wild‐type (WT) mice were placed on low‐fat diet (LFD) or high‐fat diet (HFD) for 16 weeks. CCR7 deficiency did not impact HFD‐induced weight gain, hepatic steatosis, or glucose intolerance. Although lean CCR7(−/−) mice had an increased proportion of alternatively activated ATMs, there were no differences in ATM accumulation or polarization between HFD‐fed CCR7(−/−) mice and their WT counterparts. However, CCR7 deficiency did lead to the preferential accumulation of CD8(+) ATT cells, which was further exacerbated by HFD feeding. Finally, expression of inflammatory cytokines/chemokines, such as Tnf, Il6, Il1β, Ccl2, and Ccl3, was equally elevated in AT by HFD feeding in CCR7(−/−) and WT mice, while Ifng and Il18 were elevated by HFD feeding in CCR7(−/−) but not in WT mice. Together, these data suggest that CCR7 plays a role in CD8(+) ATT cell egress, but does not influence ATM accumulation or the metabolic impact of diet‐induced obesity. John Wiley and Sons Inc. 2016-09-21 /pmc/articles/PMC5037919/ /pubmed/27655794 http://dx.doi.org/10.14814/phy2.12971 Text en © 2016 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of the American Physiological Society and The Physiological Society. This is an open access article under the terms of the Creative Commons Attribution (http://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Research Orr, Jeb S. Kennedy, Arion J. Hill, Andrea A. Anderson‐Baucum, Emily K. Hubler, Merla J. Hasty, Alyssa H. CC‐chemokine receptor 7 (CCR7) deficiency alters adipose tissue leukocyte populations in mice |
title |
CC‐chemokine receptor 7 (CCR7) deficiency alters adipose tissue leukocyte populations in mice |
title_full |
CC‐chemokine receptor 7 (CCR7) deficiency alters adipose tissue leukocyte populations in mice |
title_fullStr |
CC‐chemokine receptor 7 (CCR7) deficiency alters adipose tissue leukocyte populations in mice |
title_full_unstemmed |
CC‐chemokine receptor 7 (CCR7) deficiency alters adipose tissue leukocyte populations in mice |
title_short |
CC‐chemokine receptor 7 (CCR7) deficiency alters adipose tissue leukocyte populations in mice |
title_sort | cc‐chemokine receptor 7 (ccr7) deficiency alters adipose tissue leukocyte populations in mice |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5037919/ https://www.ncbi.nlm.nih.gov/pubmed/27655794 http://dx.doi.org/10.14814/phy2.12971 |
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