High salt aggravates renal inflammation via promoting pro-inflammatory macrophage in 5/6-nephrectomized rat

The increasing incident of chronic kidney disease (CKD) in recent years might be related to a change in dietary habits, known as excessive salt intake. Given excessive salt promotes pathogenic T cells responses. Since the importance of macrophage in the development of CKD, we addressed the effect of...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Life sciences (1973) 2021-06, Vol.274, p.119109, Article 119109
Hauptverfasser: Liu, Yang, Dai, Xiaoyan, Yang, Shaohua, Peng, Yan, Hou, Fanfan, Zhou, Qiugen
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
container_end_page
container_issue
container_start_page 119109
container_title Life sciences (1973)
container_volume 274
creator Liu, Yang
Dai, Xiaoyan
Yang, Shaohua
Peng, Yan
Hou, Fanfan
Zhou, Qiugen
description The increasing incident of chronic kidney disease (CKD) in recent years might be related to a change in dietary habits, known as excessive salt intake. Given excessive salt promotes pathogenic T cells responses. Since the importance of macrophage in the development of CKD, we addressed the effect of high salt loading on in a rat CKD model. We observed that 5/6Nx rats receiving a high salt diet showed strongly enhanced macrophage infiltration and activation in the renal tissue accompanied by deteriorated renal inflammation. Then we used the microarray expression profiling to detect the effect of additional Nacl on peritoneal macrophage derived from 5/6Nx. The NaCl treatment of macrophage extracted from 5/6Nx rat elicited a strong pro-inflammatory phenotype characterized by enhanced proinflammatory cytokine production, increased expression of molecules mainly involved in immune response process. This NaCl-induced pro-inflammatory macrophage phenotype was accompanied by increased phosphorylation of STAT1. Taken together, our study demonstrated that high salt intake promotes immune activation of macrophages through the STAT1 independently and exacerbates the kidney accompanied by promotion of inflammation. Thus, changes in diet may provide a novel strategy for the prevention or amelioration of CKD.
doi_str_mv 10.1016/j.lfs.2021.119109
format Article
fullrecord <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_journals_2519042326</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S0024320521000941</els_id><sourcerecordid>2519042326</sourcerecordid><originalsourceid>FETCH-LOGICAL-c381t-fea0c3006e1545da8b280f89516c63c6dc3025841c45c6acff772bf8f5e334b93</originalsourceid><addsrcrecordid>eNp9kE9rGzEQxUVoSFwnH6CXIuh5nRlpJe_SUwlJXTD00pyFrB2t5e4fV1ob3E8fGac59jQD895j3o-xTwgLBNQPu0Xn00KAwAVijVBfsRlWy7oALfEDmwGIspAC1C37mNIOAJRayht2K6VCKWs5Y79Xod3yZLuJ27aN9mgnSjzSYDseBt_ZvrdTGAd-DJbv49iPUxja81a8n8d44r11cdxvbUvZxtWDLgbabyO5aezDX2p4tNMdu_a2S3T_Nufs5fnp1-OqWP_8_uPx27pwssKp8GTBSQBNqErV2GojKvBVrVA7LZ1u8lGoqkRXKqet8365FBtfeUVSlptaztmXS27-8s-B0mR24yHmRskIhTWUQgqdVXhR5cdTiuTNPobexpNBMGe8ZmcyXnPGay54s-fzW_Jh01Pz7vjHMwu-XgSU-x0DRZNcoMFRE84sTDOG_8S_AuV9i4U</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2519042326</pqid></control><display><type>article</type><title>High salt aggravates renal inflammation via promoting pro-inflammatory macrophage in 5/6-nephrectomized rat</title><source>MEDLINE</source><source>Elsevier ScienceDirect Journals</source><creator>Liu, Yang ; Dai, Xiaoyan ; Yang, Shaohua ; Peng, Yan ; Hou, Fanfan ; Zhou, Qiugen</creator><creatorcontrib>Liu, Yang ; Dai, Xiaoyan ; Yang, Shaohua ; Peng, Yan ; Hou, Fanfan ; Zhou, Qiugen</creatorcontrib><description>The increasing incident of chronic kidney disease (CKD) in recent years might be related to a change in dietary habits, known as excessive salt intake. Given excessive salt promotes pathogenic T cells responses. Since the importance of macrophage in the development of CKD, we addressed the effect of high salt loading on in a rat CKD model. We observed that 5/6Nx rats receiving a high salt diet showed strongly enhanced macrophage infiltration and activation in the renal tissue accompanied by deteriorated renal inflammation. Then we used the microarray expression profiling to detect the effect of additional Nacl on peritoneal macrophage derived from 5/6Nx. The NaCl treatment of macrophage extracted from 5/6Nx rat elicited a strong pro-inflammatory phenotype characterized by enhanced proinflammatory cytokine production, increased expression of molecules mainly involved in immune response process. This NaCl-induced pro-inflammatory macrophage phenotype was accompanied by increased phosphorylation of STAT1. Taken together, our study demonstrated that high salt intake promotes immune activation of macrophages through the STAT1 independently and exacerbates the kidney accompanied by promotion of inflammation. Thus, changes in diet may provide a novel strategy for the prevention or amelioration of CKD.</description><identifier>ISSN: 0024-3205</identifier><identifier>EISSN: 1879-0631</identifier><identifier>DOI: 10.1016/j.lfs.2021.119109</identifier><identifier>PMID: 33513393</identifier><language>eng</language><publisher>Netherlands: Elsevier Inc</publisher><subject>Animals ; Cell activation ; CKD ; Cytokines ; Diet ; Gene Expression Regulation ; High salt ; Immune response ; Immune system ; Inflammation ; Inflammation - chemically induced ; Inflammation - metabolism ; Inflammation - pathology ; Inflammation Mediators - metabolism ; Kidney diseases ; Kidneys ; Lymphocytes ; Lymphocytes T ; Macrophage ; Macrophages ; Macrophages - drug effects ; Macrophages - metabolism ; Macrophages - pathology ; Male ; Nephrectomy - adverse effects ; Nephritis - chemically induced ; Nephritis - metabolism ; Nephritis - pathology ; Nephritis - surgery ; Peritoneum ; Phenotypes ; Phosphorylation ; Rats ; Rats, Sprague-Dawley ; Salt ; Salt loading ; Salts ; Sodium chloride ; Sodium Chloride - toxicity ; Stat1 protein</subject><ispartof>Life sciences (1973), 2021-06, Vol.274, p.119109, Article 119109</ispartof><rights>2021 Elsevier Inc.</rights><rights>Copyright © 2021 Elsevier Inc. All rights reserved.</rights><rights>Copyright Elsevier BV Jun 1, 2021</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c381t-fea0c3006e1545da8b280f89516c63c6dc3025841c45c6acff772bf8f5e334b93</citedby><cites>FETCH-LOGICAL-c381t-fea0c3006e1545da8b280f89516c63c6dc3025841c45c6acff772bf8f5e334b93</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.lfs.2021.119109$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3536,27903,27904,45974</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33513393$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Liu, Yang</creatorcontrib><creatorcontrib>Dai, Xiaoyan</creatorcontrib><creatorcontrib>Yang, Shaohua</creatorcontrib><creatorcontrib>Peng, Yan</creatorcontrib><creatorcontrib>Hou, Fanfan</creatorcontrib><creatorcontrib>Zhou, Qiugen</creatorcontrib><title>High salt aggravates renal inflammation via promoting pro-inflammatory macrophage in 5/6-nephrectomized rat</title><title>Life sciences (1973)</title><addtitle>Life Sci</addtitle><description>The increasing incident of chronic kidney disease (CKD) in recent years might be related to a change in dietary habits, known as excessive salt intake. Given excessive salt promotes pathogenic T cells responses. Since the importance of macrophage in the development of CKD, we addressed the effect of high salt loading on in a rat CKD model. We observed that 5/6Nx rats receiving a high salt diet showed strongly enhanced macrophage infiltration and activation in the renal tissue accompanied by deteriorated renal inflammation. Then we used the microarray expression profiling to detect the effect of additional Nacl on peritoneal macrophage derived from 5/6Nx. The NaCl treatment of macrophage extracted from 5/6Nx rat elicited a strong pro-inflammatory phenotype characterized by enhanced proinflammatory cytokine production, increased expression of molecules mainly involved in immune response process. This NaCl-induced pro-inflammatory macrophage phenotype was accompanied by increased phosphorylation of STAT1. Taken together, our study demonstrated that high salt intake promotes immune activation of macrophages through the STAT1 independently and exacerbates the kidney accompanied by promotion of inflammation. Thus, changes in diet may provide a novel strategy for the prevention or amelioration of CKD.</description><subject>Animals</subject><subject>Cell activation</subject><subject>CKD</subject><subject>Cytokines</subject><subject>Diet</subject><subject>Gene Expression Regulation</subject><subject>High salt</subject><subject>Immune response</subject><subject>Immune system</subject><subject>Inflammation</subject><subject>Inflammation - chemically induced</subject><subject>Inflammation - metabolism</subject><subject>Inflammation - pathology</subject><subject>Inflammation Mediators - metabolism</subject><subject>Kidney diseases</subject><subject>Kidneys</subject><subject>Lymphocytes</subject><subject>Lymphocytes T</subject><subject>Macrophage</subject><subject>Macrophages</subject><subject>Macrophages - drug effects</subject><subject>Macrophages - metabolism</subject><subject>Macrophages - pathology</subject><subject>Male</subject><subject>Nephrectomy - adverse effects</subject><subject>Nephritis - chemically induced</subject><subject>Nephritis - metabolism</subject><subject>Nephritis - pathology</subject><subject>Nephritis - surgery</subject><subject>Peritoneum</subject><subject>Phenotypes</subject><subject>Phosphorylation</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Salt</subject><subject>Salt loading</subject><subject>Salts</subject><subject>Sodium chloride</subject><subject>Sodium Chloride - toxicity</subject><subject>Stat1 protein</subject><issn>0024-3205</issn><issn>1879-0631</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kE9rGzEQxUVoSFwnH6CXIuh5nRlpJe_SUwlJXTD00pyFrB2t5e4fV1ob3E8fGac59jQD895j3o-xTwgLBNQPu0Xn00KAwAVijVBfsRlWy7oALfEDmwGIspAC1C37mNIOAJRayht2K6VCKWs5Y79Xod3yZLuJ27aN9mgnSjzSYDseBt_ZvrdTGAd-DJbv49iPUxja81a8n8d44r11cdxvbUvZxtWDLgbabyO5aezDX2p4tNMdu_a2S3T_Nufs5fnp1-OqWP_8_uPx27pwssKp8GTBSQBNqErV2GojKvBVrVA7LZ1u8lGoqkRXKqet8365FBtfeUVSlptaztmXS27-8s-B0mR24yHmRskIhTWUQgqdVXhR5cdTiuTNPobexpNBMGe8ZmcyXnPGay54s-fzW_Jh01Pz7vjHMwu-XgSU-x0DRZNcoMFRE84sTDOG_8S_AuV9i4U</recordid><startdate>20210601</startdate><enddate>20210601</enddate><creator>Liu, Yang</creator><creator>Dai, Xiaoyan</creator><creator>Yang, Shaohua</creator><creator>Peng, Yan</creator><creator>Hou, Fanfan</creator><creator>Zhou, Qiugen</creator><general>Elsevier Inc</general><general>Elsevier BV</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QP</scope><scope>7QR</scope><scope>7TK</scope><scope>7U7</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>RC3</scope></search><sort><creationdate>20210601</creationdate><title>High salt aggravates renal inflammation via promoting pro-inflammatory macrophage in 5/6-nephrectomized rat</title><author>Liu, Yang ; Dai, Xiaoyan ; Yang, Shaohua ; Peng, Yan ; Hou, Fanfan ; Zhou, Qiugen</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c381t-fea0c3006e1545da8b280f89516c63c6dc3025841c45c6acff772bf8f5e334b93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Animals</topic><topic>Cell activation</topic><topic>CKD</topic><topic>Cytokines</topic><topic>Diet</topic><topic>Gene Expression Regulation</topic><topic>High salt</topic><topic>Immune response</topic><topic>Immune system</topic><topic>Inflammation</topic><topic>Inflammation - chemically induced</topic><topic>Inflammation - metabolism</topic><topic>Inflammation - pathology</topic><topic>Inflammation Mediators - metabolism</topic><topic>Kidney diseases</topic><topic>Kidneys</topic><topic>Lymphocytes</topic><topic>Lymphocytes T</topic><topic>Macrophage</topic><topic>Macrophages</topic><topic>Macrophages - drug effects</topic><topic>Macrophages - metabolism</topic><topic>Macrophages - pathology</topic><topic>Male</topic><topic>Nephrectomy - adverse effects</topic><topic>Nephritis - chemically induced</topic><topic>Nephritis - metabolism</topic><topic>Nephritis - pathology</topic><topic>Nephritis - surgery</topic><topic>Peritoneum</topic><topic>Phenotypes</topic><topic>Phosphorylation</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Salt</topic><topic>Salt loading</topic><topic>Salts</topic><topic>Sodium chloride</topic><topic>Sodium Chloride - toxicity</topic><topic>Stat1 protein</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Liu, Yang</creatorcontrib><creatorcontrib>Dai, Xiaoyan</creatorcontrib><creatorcontrib>Yang, Shaohua</creatorcontrib><creatorcontrib>Peng, Yan</creatorcontrib><creatorcontrib>Hou, Fanfan</creatorcontrib><creatorcontrib>Zhou, Qiugen</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium &amp; Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><jtitle>Life sciences (1973)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Liu, Yang</au><au>Dai, Xiaoyan</au><au>Yang, Shaohua</au><au>Peng, Yan</au><au>Hou, Fanfan</au><au>Zhou, Qiugen</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>High salt aggravates renal inflammation via promoting pro-inflammatory macrophage in 5/6-nephrectomized rat</atitle><jtitle>Life sciences (1973)</jtitle><addtitle>Life Sci</addtitle><date>2021-06-01</date><risdate>2021</risdate><volume>274</volume><spage>119109</spage><pages>119109-</pages><artnum>119109</artnum><issn>0024-3205</issn><eissn>1879-0631</eissn><abstract>The increasing incident of chronic kidney disease (CKD) in recent years might be related to a change in dietary habits, known as excessive salt intake. Given excessive salt promotes pathogenic T cells responses. Since the importance of macrophage in the development of CKD, we addressed the effect of high salt loading on in a rat CKD model. We observed that 5/6Nx rats receiving a high salt diet showed strongly enhanced macrophage infiltration and activation in the renal tissue accompanied by deteriorated renal inflammation. Then we used the microarray expression profiling to detect the effect of additional Nacl on peritoneal macrophage derived from 5/6Nx. The NaCl treatment of macrophage extracted from 5/6Nx rat elicited a strong pro-inflammatory phenotype characterized by enhanced proinflammatory cytokine production, increased expression of molecules mainly involved in immune response process. This NaCl-induced pro-inflammatory macrophage phenotype was accompanied by increased phosphorylation of STAT1. Taken together, our study demonstrated that high salt intake promotes immune activation of macrophages through the STAT1 independently and exacerbates the kidney accompanied by promotion of inflammation. Thus, changes in diet may provide a novel strategy for the prevention or amelioration of CKD.</abstract><cop>Netherlands</cop><pub>Elsevier Inc</pub><pmid>33513393</pmid><doi>10.1016/j.lfs.2021.119109</doi></addata></record>
fulltext fulltext
identifier ISSN: 0024-3205
ispartof Life sciences (1973), 2021-06, Vol.274, p.119109, Article 119109
issn 0024-3205
1879-0631
language eng
recordid cdi_proquest_journals_2519042326
source MEDLINE; Elsevier ScienceDirect Journals
subjects Animals
Cell activation
CKD
Cytokines
Diet
Gene Expression Regulation
High salt
Immune response
Immune system
Inflammation
Inflammation - chemically induced
Inflammation - metabolism
Inflammation - pathology
Inflammation Mediators - metabolism
Kidney diseases
Kidneys
Lymphocytes
Lymphocytes T
Macrophage
Macrophages
Macrophages - drug effects
Macrophages - metabolism
Macrophages - pathology
Male
Nephrectomy - adverse effects
Nephritis - chemically induced
Nephritis - metabolism
Nephritis - pathology
Nephritis - surgery
Peritoneum
Phenotypes
Phosphorylation
Rats
Rats, Sprague-Dawley
Salt
Salt loading
Salts
Sodium chloride
Sodium Chloride - toxicity
Stat1 protein
title High salt aggravates renal inflammation via promoting pro-inflammatory macrophage in 5/6-nephrectomized rat
url https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-22T04%3A28%3A31IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=High%20salt%20aggravates%20renal%20inflammation%20via%20promoting%20pro-inflammatory%20macrophage%20in%205/6-nephrectomized%20rat&rft.jtitle=Life%20sciences%20(1973)&rft.au=Liu,%20Yang&rft.date=2021-06-01&rft.volume=274&rft.spage=119109&rft.pages=119109-&rft.artnum=119109&rft.issn=0024-3205&rft.eissn=1879-0631&rft_id=info:doi/10.1016/j.lfs.2021.119109&rft_dat=%3Cproquest_cross%3E2519042326%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2519042326&rft_id=info:pmid/33513393&rft_els_id=S0024320521000941&rfr_iscdi=true