Aging Reduces the Expression of Lung CINC and MCP-1 mRNA in a P. aeruginosa Rat Model of Infection
We investigated dynamic changes of inflammatory cell infiltration and expression of cytokine-induced neutrophil chemoattractant (CINC) and monocyte chemoattractant protein-1 (MCP-1) mRNA in aged rats with Pseudomonas aeruginosa pulmonary infection. Disease manifestation and lung tissue pathology (le...
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| Veröffentlicht in: | Inflammation 2014-06, Vol.37 (3), p.933-941 |
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| creator | Wen, Jie Li, Cheng-Mei Gu, Li Yin, Shao-jun Li, Wei Yang, Rong |
| description | We investigated dynamic changes of inflammatory cell infiltration and expression of cytokine-induced neutrophil chemoattractant (CINC) and monocyte chemoattractant protein-1 (MCP-1) mRNA in aged rats with
Pseudomonas aeruginosa
pulmonary infection. Disease manifestation and lung tissue pathology (lesion dispersion, inflammatory reactions, tissue edema and bleeding) were more severe in aged rats than young rats. At various time points, lung tissue polymorphonuclear neutrophil and mononuclear macrophage numbers were lower in the aged group than the young group (
P
< 0.05), and at 24 h there was no difference in mononuclear macrophage numbers. After inoculation with
P. aeruginosa
, CINC and MCP-1 mRNA expression increased in both groups, but the peak lagged in old rats compared with young. Thus, aging can reduce the expression of CINC and MCP-1 mRNA in lung tissues, and reduce the infiltration of neutrophils and monocyte–macrophages induced by CINC and MCP-1. This might lead to increased risk of pneumonia in elderly patients. |
| doi_str_mv | 10.1007/s10753-014-9813-5 |
| format | Article |
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Pseudomonas aeruginosa
pulmonary infection. Disease manifestation and lung tissue pathology (lesion dispersion, inflammatory reactions, tissue edema and bleeding) were more severe in aged rats than young rats. At various time points, lung tissue polymorphonuclear neutrophil and mononuclear macrophage numbers were lower in the aged group than the young group (
P
< 0.05), and at 24 h there was no difference in mononuclear macrophage numbers. After inoculation with
P. aeruginosa
, CINC and MCP-1 mRNA expression increased in both groups, but the peak lagged in old rats compared with young. Thus, aging can reduce the expression of CINC and MCP-1 mRNA in lung tissues, and reduce the infiltration of neutrophils and monocyte–macrophages induced by CINC and MCP-1. This might lead to increased risk of pneumonia in elderly patients.</description><identifier>ISSN: 0360-3997</identifier><identifier>EISSN: 1573-2576</identifier><identifier>DOI: 10.1007/s10753-014-9813-5</identifier><identifier>PMID: 24464584</identifier><identifier>CODEN: INFLD4</identifier><language>eng</language><publisher>Boston: Springer US</publisher><subject>Age Factors ; Aging ; Animals ; Bacterial Load - immunology ; Biomedical and Life Sciences ; Biomedicine ; Chemokine CCL2 - biosynthesis ; Chemokine CCL2 - genetics ; Chemokine CXCL1 - biosynthesis ; Chemokine CXCL1 - genetics ; Immunology ; Inflammation - immunology ; Inflammation - microbiology ; Internal Medicine ; Lung - microbiology ; Lung - pathology ; Macrophages - immunology ; Male ; Neutrophils - immunology ; Pathology ; Pharmacology/Toxicology ; Pseudomonas aeruginosa ; Pseudomonas aeruginosa - pathogenicity ; Pseudomonas Infections - epidemiology ; Rats ; Rats, Sprague-Dawley ; Rheumatology ; Risk ; RNA, Messenger</subject><ispartof>Inflammation, 2014-06, Vol.37 (3), p.933-941</ispartof><rights>The Author(s) 2014</rights><rights>Springer Science+Business Media New York 2014</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c503t-e39a9ccf6d450602b7eaec57684bc7da0f4c08239210520866bdc1c870a897563</citedby><cites>FETCH-LOGICAL-c503t-e39a9ccf6d450602b7eaec57684bc7da0f4c08239210520866bdc1c870a897563</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s10753-014-9813-5$$EPDF$$P50$$Gspringer$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10753-014-9813-5$$EHTML$$P50$$Gspringer$$Hfree_for_read</linktohtml><link.rule.ids>230,314,778,782,883,27911,27912,41475,42544,51306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24464584$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wen, Jie</creatorcontrib><creatorcontrib>Li, Cheng-Mei</creatorcontrib><creatorcontrib>Gu, Li</creatorcontrib><creatorcontrib>Yin, Shao-jun</creatorcontrib><creatorcontrib>Li, Wei</creatorcontrib><creatorcontrib>Yang, Rong</creatorcontrib><title>Aging Reduces the Expression of Lung CINC and MCP-1 mRNA in a P. aeruginosa Rat Model of Infection</title><title>Inflammation</title><addtitle>Inflammation</addtitle><addtitle>Inflammation</addtitle><description>We investigated dynamic changes of inflammatory cell infiltration and expression of cytokine-induced neutrophil chemoattractant (CINC) and monocyte chemoattractant protein-1 (MCP-1) mRNA in aged rats with
Pseudomonas aeruginosa
pulmonary infection. Disease manifestation and lung tissue pathology (lesion dispersion, inflammatory reactions, tissue edema and bleeding) were more severe in aged rats than young rats. At various time points, lung tissue polymorphonuclear neutrophil and mononuclear macrophage numbers were lower in the aged group than the young group (
P
< 0.05), and at 24 h there was no difference in mononuclear macrophage numbers. After inoculation with
P. aeruginosa
, CINC and MCP-1 mRNA expression increased in both groups, but the peak lagged in old rats compared with young. Thus, aging can reduce the expression of CINC and MCP-1 mRNA in lung tissues, and reduce the infiltration of neutrophils and monocyte–macrophages induced by CINC and MCP-1. This might lead to increased risk of pneumonia in elderly patients.</description><subject>Age Factors</subject><subject>Aging</subject><subject>Animals</subject><subject>Bacterial Load - immunology</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Chemokine CCL2 - biosynthesis</subject><subject>Chemokine CCL2 - genetics</subject><subject>Chemokine CXCL1 - biosynthesis</subject><subject>Chemokine CXCL1 - genetics</subject><subject>Immunology</subject><subject>Inflammation - immunology</subject><subject>Inflammation - microbiology</subject><subject>Internal Medicine</subject><subject>Lung - microbiology</subject><subject>Lung - pathology</subject><subject>Macrophages - immunology</subject><subject>Male</subject><subject>Neutrophils - immunology</subject><subject>Pathology</subject><subject>Pharmacology/Toxicology</subject><subject>Pseudomonas aeruginosa</subject><subject>Pseudomonas aeruginosa - pathogenicity</subject><subject>Pseudomonas Infections - epidemiology</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Rheumatology</subject><subject>Risk</subject><subject>RNA, Messenger</subject><issn>0360-3997</issn><issn>1573-2576</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNqNkU1v1DAQhi0EokvhB3BBlrhwSRl_OxekVdTCSttSreBsOY6zTZW1FztB8O_rZUtVkJA4-TDPPJ6ZF6HXBM4IgHqfCSjBKiC8qjVhlXiCFkQoVlGh5FO0ACahYnWtTtCLnG8BQNeaPUcnlHPJheYL1C63Q9jije9m5zOebjw-_7FPPuchBhx7vJ5LuVldNdiGDl821xXBu83VEg8BW3x9hq1Pc3HEbPHGTvgydn48NK5C791ULC_Rs96O2b-6f0_R14vzL82nav3546pZrisngE2VZ7WtnetlxwVIoK3y1ruyiOatU52FnjvQlNWUgKCgpWw7R5xWYHWthGSn6MPRu5_bne-cD1Oyo9mnYWfTTxPtYP6shOHGbON3w4FRyXQRvLsXpPht9nkyuyE7P442-DhnQwTjmsmaif9AqdaKaUUK-vYv9DbOKZRL_KIoCAasUORIuRRzTr5_mJuAOYRtjmGbErY5hG0OQ7x5vPBDx-90C0CPQC6lsPXp0df_tN4BEfmxbQ</recordid><startdate>20140601</startdate><enddate>20140601</enddate><creator>Wen, Jie</creator><creator>Li, Cheng-Mei</creator><creator>Gu, Li</creator><creator>Yin, Shao-jun</creator><creator>Li, Wei</creator><creator>Yang, Rong</creator><general>Springer US</general><general>Springer Nature B.V</general><scope>C6C</scope><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>3V.</scope><scope>7T5</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20140601</creationdate><title>Aging Reduces the Expression of Lung CINC and MCP-1 mRNA in a P. aeruginosa Rat Model of Infection</title><author>Wen, Jie ; Li, Cheng-Mei ; Gu, Li ; Yin, Shao-jun ; Li, Wei ; Yang, Rong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c503t-e39a9ccf6d450602b7eaec57684bc7da0f4c08239210520866bdc1c870a897563</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Age Factors</topic><topic>Aging</topic><topic>Animals</topic><topic>Bacterial Load - immunology</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Chemokine CCL2 - biosynthesis</topic><topic>Chemokine CCL2 - genetics</topic><topic>Chemokine CXCL1 - biosynthesis</topic><topic>Chemokine CXCL1 - genetics</topic><topic>Immunology</topic><topic>Inflammation - immunology</topic><topic>Inflammation - microbiology</topic><topic>Internal Medicine</topic><topic>Lung - microbiology</topic><topic>Lung - pathology</topic><topic>Macrophages - immunology</topic><topic>Male</topic><topic>Neutrophils - immunology</topic><topic>Pathology</topic><topic>Pharmacology/Toxicology</topic><topic>Pseudomonas aeruginosa</topic><topic>Pseudomonas aeruginosa - pathogenicity</topic><topic>Pseudomonas Infections - epidemiology</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Rheumatology</topic><topic>Risk</topic><topic>RNA, Messenger</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wen, Jie</creatorcontrib><creatorcontrib>Li, Cheng-Mei</creatorcontrib><creatorcontrib>Gu, Li</creatorcontrib><creatorcontrib>Yin, Shao-jun</creatorcontrib><creatorcontrib>Li, Wei</creatorcontrib><creatorcontrib>Yang, Rong</creatorcontrib><collection>Springer Nature OA Free Journals</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</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</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical 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>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Inflammation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wen, Jie</au><au>Li, Cheng-Mei</au><au>Gu, Li</au><au>Yin, Shao-jun</au><au>Li, Wei</au><au>Yang, Rong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Aging Reduces the Expression of Lung CINC and MCP-1 mRNA in a P. aeruginosa Rat Model of Infection</atitle><jtitle>Inflammation</jtitle><stitle>Inflammation</stitle><addtitle>Inflammation</addtitle><date>2014-06-01</date><risdate>2014</risdate><volume>37</volume><issue>3</issue><spage>933</spage><epage>941</epage><pages>933-941</pages><issn>0360-3997</issn><eissn>1573-2576</eissn><coden>INFLD4</coden><abstract>We investigated dynamic changes of inflammatory cell infiltration and expression of cytokine-induced neutrophil chemoattractant (CINC) and monocyte chemoattractant protein-1 (MCP-1) mRNA in aged rats with
Pseudomonas aeruginosa
pulmonary infection. Disease manifestation and lung tissue pathology (lesion dispersion, inflammatory reactions, tissue edema and bleeding) were more severe in aged rats than young rats. At various time points, lung tissue polymorphonuclear neutrophil and mononuclear macrophage numbers were lower in the aged group than the young group (
P
< 0.05), and at 24 h there was no difference in mononuclear macrophage numbers. After inoculation with
P. aeruginosa
, CINC and MCP-1 mRNA expression increased in both groups, but the peak lagged in old rats compared with young. Thus, aging can reduce the expression of CINC and MCP-1 mRNA in lung tissues, and reduce the infiltration of neutrophils and monocyte–macrophages induced by CINC and MCP-1. This might lead to increased risk of pneumonia in elderly patients.</abstract><cop>Boston</cop><pub>Springer US</pub><pmid>24464584</pmid><doi>10.1007/s10753-014-9813-5</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Inflammation, 2014-06, Vol.37 (3), p.933-941 |
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| source | MEDLINE; Springer Nature - Complete Springer Journals |
| subjects | Age Factors Aging Animals Bacterial Load - immunology Biomedical and Life Sciences Biomedicine Chemokine CCL2 - biosynthesis Chemokine CCL2 - genetics Chemokine CXCL1 - biosynthesis Chemokine CXCL1 - genetics Immunology Inflammation - immunology Inflammation - microbiology Internal Medicine Lung - microbiology Lung - pathology Macrophages - immunology Male Neutrophils - immunology Pathology Pharmacology/Toxicology Pseudomonas aeruginosa Pseudomonas aeruginosa - pathogenicity Pseudomonas Infections - epidemiology Rats Rats, Sprague-Dawley Rheumatology Risk RNA, Messenger |
| title | Aging Reduces the Expression of Lung CINC and MCP-1 mRNA in a P. aeruginosa Rat Model of Infection |
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