Salt-Sensitive Ileal Microbiota Plays a Role in Atrial Natriuretic Peptide Deficiency-Induced Cardiac Injury
Atrial natriuretic peptide (ANP) activity deficiency contributes to salt-sensitive hypertension in humans and mice. However, the role of ileal microbiota in salt sensitivity in ANP deficiency-related cardiac injury has not been investigated yet. This study used ANP−/− mice to analyze the role of the...
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Veröffentlicht in: | Nutrients 2022-07, Vol.14 (15), p.3129 |
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creator | Li, Siqi Chen, Sishuo Nie, Min Wen, Lijing Zou, Bin Zhang, Lingyu Xie, Jingzhou Ser, Hooi-Leng Lee, Learn-Han Wang, Shunyi Lin, Caixia Pathak, Janak L. Zhou, Weijie Miao, Ji Wang, Lijing Zheng, Lingyun |
description | Atrial natriuretic peptide (ANP) activity deficiency contributes to salt-sensitive hypertension in humans and mice. However, the role of ileal microbiota in salt sensitivity in ANP deficiency-related cardiac injury has not been investigated yet. This study used ANP−/− mice to analyze the role of the salt-sensitive ileal microbiome on cardiac injury. ANP−/− mice showed an increase in blood pressure (BP), the heart weight/body weight (HW/BW) ratio, and cardiac hypertrophy compared with wild-type (WT) mice. ANP deficiency did not impact the histological structure but reduced occludin expression in the ileum. Antibiotics significantly relieved BP and cardiac hypertrophy in ANP−/− mice. A high-salt diet (HSD) increased BP, the HW/BW ratio, and cardiac hypertrophy/fibrosis in WT and ANP−/− mice, and an HSD treatment in ANP−/− mice exacerbated these cardiac parameters. The HSD markedly decreased muscularis layer thickening, villus length, and numbers of Paneth and goblet cells in the ileum of WT and ANP−/− mice. Furthermore, the HSD increased the level of TLR4 and IL-1β in ANP−/− mice ileum compared with WT mice. Antibiotics reduced the HW/BW ratio, cardiac hypertrophy/fibrosis, and the level of TLR4 and IL-1β in the ileum, and rescued the muscularis layer thickening, villus length, and numbers of Paneth and goblet cells in the ileum of HSD-ANP−/− mice. Importantly, ANP deficiency induced the colonization of Burkholderiales bacterium YL45, Lactobacillus johnsonii, and Lactobacillus reuteri in the ileum on the NSD diet, which was only observed in HSD-induced WT mice but not in WT mice on the NSD. Besides, the HSD significantly enhanced the sum of the percentage of the colonization of Burkholderiales bacterium YL45, Lactobacillus johnsonii, and Lactobacillus reuteri in the ileum of ANP−/− mice. Ileal microbiota transfer (IMT) from ANP−/− mice to healthy C57BL/6J mice drove Lactobacillus johnsonii and Lactobacillus reuteri colonization in the ileum, which manifested an increase in BP, the HW/BW ratio, cardiac hypertrophy, and ileal pathology compared with IMT from WT mice. The HSD in C57BL/6J mice with IMT from ANP−/− mice drove the colonization of Burkholderiales bacterium YL45, Lactobacillus johnsonii, and Lactobacillus reuteri in the ileum and further exacerbated the cardiac and ileal pathology. Our results suggest that salt-sensitive ileal microbiota is probably related to ANP deficiency-induced cardiac injury. |
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fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_9370783</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2702180614</sourcerecordid><originalsourceid>FETCH-LOGICAL-c416t-b2fe821ead76f0e56d6ade1a2efe2bea63386212a3584a3b85a7e920e7c1cacf3</originalsourceid><addsrcrecordid>eNqNkU9r3DAQxUVpaUKSSz-BoJdQcCtpbNm-FMLmTxeSJiTtWYzlcatFK28lObDfPl4S2iSnzuUNzI_H8B5jH6T4DNCKL2GSpaxAqvYN21eiVoXWJbx9tu-xo5RWYje1qDW8Z3tQtZUGofeZv0OfizsKyWV3T3zpCT2_cjaOnRsz8huP28SR346euAv8JEc3E99x1ilSdpbf0Ca7nvgpDc46CnZbLEM_Wer5AmPv0PJlWE1xe8jeDegTHT3pAft5fvZj8a24vL5YLk4uC1tKnYtODdQoSdjXehBU6V5jTxIVDaQ6Qg3QaCUVQtWUCF1TYU2tElRbadEOcMC-Pvpupm5NvaWQI3qziW6NcWtGdOblJbjf5td4b1qYE2pgNjh-Mojjn4lSNmuXLHmPgcYpGVXLBrRulPgPVCjZCC3LGf34Cl2NUwxzEjtK1GWpQc3Up0dqriClSMPfv6Uwu8rNv8rhAdbinYQ</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2700744632</pqid></control><display><type>article</type><title>Salt-Sensitive Ileal Microbiota Plays a Role in Atrial Natriuretic Peptide Deficiency-Induced Cardiac Injury</title><source>MDPI - Multidisciplinary Digital Publishing Institute</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>PubMed Central</source><source>PubMed Central Open Access</source><creator>Li, Siqi ; Chen, Sishuo ; Nie, Min ; Wen, Lijing ; Zou, Bin ; Zhang, Lingyu ; Xie, Jingzhou ; Ser, Hooi-Leng ; Lee, Learn-Han ; Wang, Shunyi ; Lin, Caixia ; Pathak, Janak L. ; Zhou, Weijie ; Miao, Ji ; Wang, Lijing ; Zheng, Lingyun</creator><creatorcontrib>Li, Siqi ; Chen, Sishuo ; Nie, Min ; Wen, Lijing ; Zou, Bin ; Zhang, Lingyu ; Xie, Jingzhou ; Ser, Hooi-Leng ; Lee, Learn-Han ; Wang, Shunyi ; Lin, Caixia ; Pathak, Janak L. ; Zhou, Weijie ; Miao, Ji ; Wang, Lijing ; Zheng, Lingyun</creatorcontrib><description>Atrial natriuretic peptide (ANP) activity deficiency contributes to salt-sensitive hypertension in humans and mice. However, the role of ileal microbiota in salt sensitivity in ANP deficiency-related cardiac injury has not been investigated yet. This study used ANP−/− mice to analyze the role of the salt-sensitive ileal microbiome on cardiac injury. ANP−/− mice showed an increase in blood pressure (BP), the heart weight/body weight (HW/BW) ratio, and cardiac hypertrophy compared with wild-type (WT) mice. ANP deficiency did not impact the histological structure but reduced occludin expression in the ileum. Antibiotics significantly relieved BP and cardiac hypertrophy in ANP−/− mice. A high-salt diet (HSD) increased BP, the HW/BW ratio, and cardiac hypertrophy/fibrosis in WT and ANP−/− mice, and an HSD treatment in ANP−/− mice exacerbated these cardiac parameters. The HSD markedly decreased muscularis layer thickening, villus length, and numbers of Paneth and goblet cells in the ileum of WT and ANP−/− mice. Furthermore, the HSD increased the level of TLR4 and IL-1β in ANP−/− mice ileum compared with WT mice. Antibiotics reduced the HW/BW ratio, cardiac hypertrophy/fibrosis, and the level of TLR4 and IL-1β in the ileum, and rescued the muscularis layer thickening, villus length, and numbers of Paneth and goblet cells in the ileum of HSD-ANP−/− mice. Importantly, ANP deficiency induced the colonization of Burkholderiales bacterium YL45, Lactobacillus johnsonii, and Lactobacillus reuteri in the ileum on the NSD diet, which was only observed in HSD-induced WT mice but not in WT mice on the NSD. Besides, the HSD significantly enhanced the sum of the percentage of the colonization of Burkholderiales bacterium YL45, Lactobacillus johnsonii, and Lactobacillus reuteri in the ileum of ANP−/− mice. Ileal microbiota transfer (IMT) from ANP−/− mice to healthy C57BL/6J mice drove Lactobacillus johnsonii and Lactobacillus reuteri colonization in the ileum, which manifested an increase in BP, the HW/BW ratio, cardiac hypertrophy, and ileal pathology compared with IMT from WT mice. The HSD in C57BL/6J mice with IMT from ANP−/− mice drove the colonization of Burkholderiales bacterium YL45, Lactobacillus johnsonii, and Lactobacillus reuteri in the ileum and further exacerbated the cardiac and ileal pathology. Our results suggest that salt-sensitive ileal microbiota is probably related to ANP deficiency-induced cardiac injury.</description><identifier>ISSN: 2072-6643</identifier><identifier>EISSN: 2072-6643</identifier><identifier>DOI: 10.3390/nu14153129</identifier><identifier>PMID: 35956306</identifier><language>eng</language><publisher>Basel: MDPI AG</publisher><subject>Antibiotics ; Atrial natriuretic peptide ; Bacteria ; Blood pressure ; Body weight ; Burkholderiales ; Colon ; Colonization ; Diet ; Drinking water ; Experiments ; Feces ; Fibrosis ; Goblet cells ; Heart ; histology ; Homeostasis ; Hypertension ; Hypertrophy ; IL-1β ; Ileum ; Injury analysis ; Laboratory animals ; Lactobacillus johnsonii ; Lactobacillus reuteri ; microbiome ; Microbiomes ; Microbiota ; occludins ; Pathology ; Peptides ; Rodents ; Salt ; Salts ; Small intestine ; Thickening ; TLR4 protein ; Toll-like receptors ; villi ; Villus</subject><ispartof>Nutrients, 2022-07, Vol.14 (15), p.3129</ispartof><rights>2022 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2022 by the authors. 2022</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c416t-b2fe821ead76f0e56d6ade1a2efe2bea63386212a3584a3b85a7e920e7c1cacf3</citedby><cites>FETCH-LOGICAL-c416t-b2fe821ead76f0e56d6ade1a2efe2bea63386212a3584a3b85a7e920e7c1cacf3</cites><orcidid>0000-0003-3815-7436 ; 0000-0002-3199-084X ; 0000-0003-2576-443X ; 0000-0002-8589-7456 ; 0000-0001-9243-9923 ; 0000-0003-0869-4492</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9370783/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9370783/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids></links><search><creatorcontrib>Li, Siqi</creatorcontrib><creatorcontrib>Chen, Sishuo</creatorcontrib><creatorcontrib>Nie, Min</creatorcontrib><creatorcontrib>Wen, Lijing</creatorcontrib><creatorcontrib>Zou, Bin</creatorcontrib><creatorcontrib>Zhang, Lingyu</creatorcontrib><creatorcontrib>Xie, Jingzhou</creatorcontrib><creatorcontrib>Ser, Hooi-Leng</creatorcontrib><creatorcontrib>Lee, Learn-Han</creatorcontrib><creatorcontrib>Wang, Shunyi</creatorcontrib><creatorcontrib>Lin, Caixia</creatorcontrib><creatorcontrib>Pathak, Janak L.</creatorcontrib><creatorcontrib>Zhou, Weijie</creatorcontrib><creatorcontrib>Miao, Ji</creatorcontrib><creatorcontrib>Wang, Lijing</creatorcontrib><creatorcontrib>Zheng, Lingyun</creatorcontrib><title>Salt-Sensitive Ileal Microbiota Plays a Role in Atrial Natriuretic Peptide Deficiency-Induced Cardiac Injury</title><title>Nutrients</title><description>Atrial natriuretic peptide (ANP) activity deficiency contributes to salt-sensitive hypertension in humans and mice. However, the role of ileal microbiota in salt sensitivity in ANP deficiency-related cardiac injury has not been investigated yet. This study used ANP−/− mice to analyze the role of the salt-sensitive ileal microbiome on cardiac injury. ANP−/− mice showed an increase in blood pressure (BP), the heart weight/body weight (HW/BW) ratio, and cardiac hypertrophy compared with wild-type (WT) mice. ANP deficiency did not impact the histological structure but reduced occludin expression in the ileum. Antibiotics significantly relieved BP and cardiac hypertrophy in ANP−/− mice. A high-salt diet (HSD) increased BP, the HW/BW ratio, and cardiac hypertrophy/fibrosis in WT and ANP−/− mice, and an HSD treatment in ANP−/− mice exacerbated these cardiac parameters. The HSD markedly decreased muscularis layer thickening, villus length, and numbers of Paneth and goblet cells in the ileum of WT and ANP−/− mice. Furthermore, the HSD increased the level of TLR4 and IL-1β in ANP−/− mice ileum compared with WT mice. Antibiotics reduced the HW/BW ratio, cardiac hypertrophy/fibrosis, and the level of TLR4 and IL-1β in the ileum, and rescued the muscularis layer thickening, villus length, and numbers of Paneth and goblet cells in the ileum of HSD-ANP−/− mice. Importantly, ANP deficiency induced the colonization of Burkholderiales bacterium YL45, Lactobacillus johnsonii, and Lactobacillus reuteri in the ileum on the NSD diet, which was only observed in HSD-induced WT mice but not in WT mice on the NSD. Besides, the HSD significantly enhanced the sum of the percentage of the colonization of Burkholderiales bacterium YL45, Lactobacillus johnsonii, and Lactobacillus reuteri in the ileum of ANP−/− mice. Ileal microbiota transfer (IMT) from ANP−/− mice to healthy C57BL/6J mice drove Lactobacillus johnsonii and Lactobacillus reuteri colonization in the ileum, which manifested an increase in BP, the HW/BW ratio, cardiac hypertrophy, and ileal pathology compared with IMT from WT mice. The HSD in C57BL/6J mice with IMT from ANP−/− mice drove the colonization of Burkholderiales bacterium YL45, Lactobacillus johnsonii, and Lactobacillus reuteri in the ileum and further exacerbated the cardiac and ileal pathology. Our results suggest that salt-sensitive ileal microbiota is probably related to ANP deficiency-induced cardiac injury.</description><subject>Antibiotics</subject><subject>Atrial natriuretic peptide</subject><subject>Bacteria</subject><subject>Blood pressure</subject><subject>Body weight</subject><subject>Burkholderiales</subject><subject>Colon</subject><subject>Colonization</subject><subject>Diet</subject><subject>Drinking water</subject><subject>Experiments</subject><subject>Feces</subject><subject>Fibrosis</subject><subject>Goblet cells</subject><subject>Heart</subject><subject>histology</subject><subject>Homeostasis</subject><subject>Hypertension</subject><subject>Hypertrophy</subject><subject>IL-1β</subject><subject>Ileum</subject><subject>Injury analysis</subject><subject>Laboratory animals</subject><subject>Lactobacillus johnsonii</subject><subject>Lactobacillus reuteri</subject><subject>microbiome</subject><subject>Microbiomes</subject><subject>Microbiota</subject><subject>occludins</subject><subject>Pathology</subject><subject>Peptides</subject><subject>Rodents</subject><subject>Salt</subject><subject>Salts</subject><subject>Small intestine</subject><subject>Thickening</subject><subject>TLR4 protein</subject><subject>Toll-like receptors</subject><subject>villi</subject><subject>Villus</subject><issn>2072-6643</issn><issn>2072-6643</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>BENPR</sourceid><recordid>eNqNkU9r3DAQxUVpaUKSSz-BoJdQcCtpbNm-FMLmTxeSJiTtWYzlcatFK28lObDfPl4S2iSnzuUNzI_H8B5jH6T4DNCKL2GSpaxAqvYN21eiVoXWJbx9tu-xo5RWYje1qDW8Z3tQtZUGofeZv0OfizsKyWV3T3zpCT2_cjaOnRsz8huP28SR346euAv8JEc3E99x1ilSdpbf0Ca7nvgpDc46CnZbLEM_Wer5AmPv0PJlWE1xe8jeDegTHT3pAft5fvZj8a24vL5YLk4uC1tKnYtODdQoSdjXehBU6V5jTxIVDaQ6Qg3QaCUVQtWUCF1TYU2tElRbadEOcMC-Pvpupm5NvaWQI3qziW6NcWtGdOblJbjf5td4b1qYE2pgNjh-Mojjn4lSNmuXLHmPgcYpGVXLBrRulPgPVCjZCC3LGf34Cl2NUwxzEjtK1GWpQc3Up0dqriClSMPfv6Uwu8rNv8rhAdbinYQ</recordid><startdate>20220729</startdate><enddate>20220729</enddate><creator>Li, Siqi</creator><creator>Chen, Sishuo</creator><creator>Nie, Min</creator><creator>Wen, Lijing</creator><creator>Zou, Bin</creator><creator>Zhang, Lingyu</creator><creator>Xie, Jingzhou</creator><creator>Ser, Hooi-Leng</creator><creator>Lee, Learn-Han</creator><creator>Wang, Shunyi</creator><creator>Lin, Caixia</creator><creator>Pathak, Janak L.</creator><creator>Zhou, Weijie</creator><creator>Miao, Ji</creator><creator>Wang, Lijing</creator><creator>Zheng, Lingyun</creator><general>MDPI AG</general><general>MDPI</general><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7TS</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>7S9</scope><scope>L.6</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0003-3815-7436</orcidid><orcidid>https://orcid.org/0000-0002-3199-084X</orcidid><orcidid>https://orcid.org/0000-0003-2576-443X</orcidid><orcidid>https://orcid.org/0000-0002-8589-7456</orcidid><orcidid>https://orcid.org/0000-0001-9243-9923</orcidid><orcidid>https://orcid.org/0000-0003-0869-4492</orcidid></search><sort><creationdate>20220729</creationdate><title>Salt-Sensitive Ileal Microbiota Plays a Role in Atrial Natriuretic Peptide Deficiency-Induced Cardiac Injury</title><author>Li, Siqi ; Chen, Sishuo ; Nie, Min ; Wen, Lijing ; Zou, Bin ; Zhang, Lingyu ; Xie, Jingzhou ; Ser, Hooi-Leng ; Lee, Learn-Han ; Wang, Shunyi ; Lin, Caixia ; Pathak, Janak L. ; Zhou, Weijie ; Miao, Ji ; Wang, Lijing ; Zheng, Lingyun</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c416t-b2fe821ead76f0e56d6ade1a2efe2bea63386212a3584a3b85a7e920e7c1cacf3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Antibiotics</topic><topic>Atrial natriuretic peptide</topic><topic>Bacteria</topic><topic>Blood pressure</topic><topic>Body weight</topic><topic>Burkholderiales</topic><topic>Colon</topic><topic>Colonization</topic><topic>Diet</topic><topic>Drinking water</topic><topic>Experiments</topic><topic>Feces</topic><topic>Fibrosis</topic><topic>Goblet cells</topic><topic>Heart</topic><topic>histology</topic><topic>Homeostasis</topic><topic>Hypertension</topic><topic>Hypertrophy</topic><topic>IL-1β</topic><topic>Ileum</topic><topic>Injury analysis</topic><topic>Laboratory animals</topic><topic>Lactobacillus johnsonii</topic><topic>Lactobacillus reuteri</topic><topic>microbiome</topic><topic>Microbiomes</topic><topic>Microbiota</topic><topic>occludins</topic><topic>Pathology</topic><topic>Peptides</topic><topic>Rodents</topic><topic>Salt</topic><topic>Salts</topic><topic>Small intestine</topic><topic>Thickening</topic><topic>TLR4 protein</topic><topic>Toll-like receptors</topic><topic>villi</topic><topic>Villus</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Li, Siqi</creatorcontrib><creatorcontrib>Chen, Sishuo</creatorcontrib><creatorcontrib>Nie, Min</creatorcontrib><creatorcontrib>Wen, Lijing</creatorcontrib><creatorcontrib>Zou, Bin</creatorcontrib><creatorcontrib>Zhang, Lingyu</creatorcontrib><creatorcontrib>Xie, Jingzhou</creatorcontrib><creatorcontrib>Ser, Hooi-Leng</creatorcontrib><creatorcontrib>Lee, Learn-Han</creatorcontrib><creatorcontrib>Wang, Shunyi</creatorcontrib><creatorcontrib>Lin, Caixia</creatorcontrib><creatorcontrib>Pathak, Janak L.</creatorcontrib><creatorcontrib>Zhou, Weijie</creatorcontrib><creatorcontrib>Miao, Ji</creatorcontrib><creatorcontrib>Wang, Lijing</creatorcontrib><creatorcontrib>Zheng, Lingyun</creatorcontrib><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Physical Education Index</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>AGRICOLA</collection><collection>AGRICOLA - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Nutrients</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, Siqi</au><au>Chen, Sishuo</au><au>Nie, Min</au><au>Wen, Lijing</au><au>Zou, Bin</au><au>Zhang, Lingyu</au><au>Xie, Jingzhou</au><au>Ser, Hooi-Leng</au><au>Lee, Learn-Han</au><au>Wang, Shunyi</au><au>Lin, Caixia</au><au>Pathak, Janak L.</au><au>Zhou, Weijie</au><au>Miao, Ji</au><au>Wang, Lijing</au><au>Zheng, Lingyun</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Salt-Sensitive Ileal Microbiota Plays a Role in Atrial Natriuretic Peptide Deficiency-Induced Cardiac Injury</atitle><jtitle>Nutrients</jtitle><date>2022-07-29</date><risdate>2022</risdate><volume>14</volume><issue>15</issue><spage>3129</spage><pages>3129-</pages><issn>2072-6643</issn><eissn>2072-6643</eissn><abstract>Atrial natriuretic peptide (ANP) activity deficiency contributes to salt-sensitive hypertension in humans and mice. However, the role of ileal microbiota in salt sensitivity in ANP deficiency-related cardiac injury has not been investigated yet. This study used ANP−/− mice to analyze the role of the salt-sensitive ileal microbiome on cardiac injury. ANP−/− mice showed an increase in blood pressure (BP), the heart weight/body weight (HW/BW) ratio, and cardiac hypertrophy compared with wild-type (WT) mice. ANP deficiency did not impact the histological structure but reduced occludin expression in the ileum. Antibiotics significantly relieved BP and cardiac hypertrophy in ANP−/− mice. A high-salt diet (HSD) increased BP, the HW/BW ratio, and cardiac hypertrophy/fibrosis in WT and ANP−/− mice, and an HSD treatment in ANP−/− mice exacerbated these cardiac parameters. The HSD markedly decreased muscularis layer thickening, villus length, and numbers of Paneth and goblet cells in the ileum of WT and ANP−/− mice. Furthermore, the HSD increased the level of TLR4 and IL-1β in ANP−/− mice ileum compared with WT mice. Antibiotics reduced the HW/BW ratio, cardiac hypertrophy/fibrosis, and the level of TLR4 and IL-1β in the ileum, and rescued the muscularis layer thickening, villus length, and numbers of Paneth and goblet cells in the ileum of HSD-ANP−/− mice. Importantly, ANP deficiency induced the colonization of Burkholderiales bacterium YL45, Lactobacillus johnsonii, and Lactobacillus reuteri in the ileum on the NSD diet, which was only observed in HSD-induced WT mice but not in WT mice on the NSD. Besides, the HSD significantly enhanced the sum of the percentage of the colonization of Burkholderiales bacterium YL45, Lactobacillus johnsonii, and Lactobacillus reuteri in the ileum of ANP−/− mice. Ileal microbiota transfer (IMT) from ANP−/− mice to healthy C57BL/6J mice drove Lactobacillus johnsonii and Lactobacillus reuteri colonization in the ileum, which manifested an increase in BP, the HW/BW ratio, cardiac hypertrophy, and ileal pathology compared with IMT from WT mice. The HSD in C57BL/6J mice with IMT from ANP−/− mice drove the colonization of Burkholderiales bacterium YL45, Lactobacillus johnsonii, and Lactobacillus reuteri in the ileum and further exacerbated the cardiac and ileal pathology. Our results suggest that salt-sensitive ileal microbiota is probably related to ANP deficiency-induced cardiac injury.</abstract><cop>Basel</cop><pub>MDPI AG</pub><pmid>35956306</pmid><doi>10.3390/nu14153129</doi><orcidid>https://orcid.org/0000-0003-3815-7436</orcidid><orcidid>https://orcid.org/0000-0002-3199-084X</orcidid><orcidid>https://orcid.org/0000-0003-2576-443X</orcidid><orcidid>https://orcid.org/0000-0002-8589-7456</orcidid><orcidid>https://orcid.org/0000-0001-9243-9923</orcidid><orcidid>https://orcid.org/0000-0003-0869-4492</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Antibiotics Atrial natriuretic peptide Bacteria Blood pressure Body weight Burkholderiales Colon Colonization Diet Drinking water Experiments Feces Fibrosis Goblet cells Heart histology Homeostasis Hypertension Hypertrophy IL-1β Ileum Injury analysis Laboratory animals Lactobacillus johnsonii Lactobacillus reuteri microbiome Microbiomes Microbiota occludins Pathology Peptides Rodents Salt Salts Small intestine Thickening TLR4 protein Toll-like receptors villi Villus |
title | Salt-Sensitive Ileal Microbiota Plays a Role in Atrial Natriuretic Peptide Deficiency-Induced Cardiac Injury |
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