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...
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Veröffentlicht in: | Life sciences (1973) 2021-06, Vol.274, p.119109, Article 119109 |
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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. |
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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 & 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> |
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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 |
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