The changes induced by cyclophosphamide in intestinal barrier and microflora in mice
Infection is one of the most commonly encountered complication during chemotherapy treatment, and recent studies showed that such infections are aroused primarily from the intestinal microflora through bacterial translocation. We aimed to investigate the alterations of mucosal barrier and colonizati...
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| Veröffentlicht in: | European journal of pharmacology 2013-08, Vol.714 (1-3), p.120-124 |
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| creator | Yang, Jin Liu, Kai-xiong Qu, Jie-ming Wang, Xiao-dan |
| description | Infection is one of the most commonly encountered complication during chemotherapy treatment, and recent studies showed that such infections are aroused primarily from the intestinal microflora through bacterial translocation. We aimed to investigate the alterations of mucosal barrier and colonization resistance in mouse treated with cyclophosphamide (CTX) to further understand the translocation mechanism. Male Balb/c mice were administered intraperitoneally with CTX at 25mg/kg, 50mg/kg and 100mg/kg for 5 days. We found that pretreatment with CTX, especially at high dose, increased the potentially pathogenic bacteria counts (Escherichia coli, enterobacteraceae, Pseudomonas and enterococci) and the intestinal permeability, which was associated with the reduction of tight junctions and adherens junctions. Our results suggested that disruption of mucosal barrier and colonization resistance may be partly responsible for the bacterial translocation during chemotherapy. Thus, modulation of mechanical mucosal barrier and colonization resistance might represent a new opportunity for applications in cancer patients to reduce infectious complications. |
| doi_str_mv | 10.1016/j.ejphar.2013.06.006 |
| format | Article |
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We aimed to investigate the alterations of mucosal barrier and colonization resistance in mouse treated with cyclophosphamide (CTX) to further understand the translocation mechanism. Male Balb/c mice were administered intraperitoneally with CTX at 25mg/kg, 50mg/kg and 100mg/kg for 5 days. We found that pretreatment with CTX, especially at high dose, increased the potentially pathogenic bacteria counts (Escherichia coli, enterobacteraceae, Pseudomonas and enterococci) and the intestinal permeability, which was associated with the reduction of tight junctions and adherens junctions. Our results suggested that disruption of mucosal barrier and colonization resistance may be partly responsible for the bacterial translocation during chemotherapy. Thus, modulation of mechanical mucosal barrier and colonization resistance might represent a new opportunity for applications in cancer patients to reduce infectious complications.</description><identifier>ISSN: 0014-2999</identifier><identifier>EISSN: 1879-0712</identifier><identifier>DOI: 10.1016/j.ejphar.2013.06.006</identifier><identifier>PMID: 23791611</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>adherens junctions ; Animals ; Antineoplastic Agents - adverse effects ; bacteria ; Bacterial translocation ; Cadherins - metabolism ; chemotherapy ; Cyclophosphamide ; Cyclophosphamide - adverse effects ; Enterococcus ; Escherichia coli ; Gene Expression Regulation - drug effects ; Intestinal microflora ; intestinal microorganisms ; Intestinal Mucosa - drug effects ; Intestinal Mucosa - microbiology ; Intestines - drug effects ; Intestines - metabolism ; Intestines - microbiology ; Male ; Mice ; Mice, Inbred BALB C ; Microbiota - drug effects ; Occludin - metabolism ; patients ; permeability ; Permeability - drug effects ; Pseudomonas ; Tight junction ; tight junctions ; Zonula Occludens-1 Protein - metabolism</subject><ispartof>European journal of pharmacology, 2013-08, Vol.714 (1-3), p.120-124</ispartof><rights>2013 Elsevier B.V.</rights><rights>Copyright © 2013 Elsevier B.V. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c386t-17992e2a8b9b000c81d79abc517536ffdd9607d09ba48136dda690bcebab69a33</citedby><cites>FETCH-LOGICAL-c386t-17992e2a8b9b000c81d79abc517536ffdd9607d09ba48136dda690bcebab69a33</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.ejphar.2013.06.006$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3548,27923,27924,45994</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23791611$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yang, Jin</creatorcontrib><creatorcontrib>Liu, Kai-xiong</creatorcontrib><creatorcontrib>Qu, Jie-ming</creatorcontrib><creatorcontrib>Wang, Xiao-dan</creatorcontrib><title>The changes induced by cyclophosphamide in intestinal barrier and microflora in mice</title><title>European journal of pharmacology</title><addtitle>Eur J Pharmacol</addtitle><description>Infection is one of the most commonly encountered complication during chemotherapy treatment, and recent studies showed that such infections are aroused primarily from the intestinal microflora through bacterial translocation. We aimed to investigate the alterations of mucosal barrier and colonization resistance in mouse treated with cyclophosphamide (CTX) to further understand the translocation mechanism. Male Balb/c mice were administered intraperitoneally with CTX at 25mg/kg, 50mg/kg and 100mg/kg for 5 days. We found that pretreatment with CTX, especially at high dose, increased the potentially pathogenic bacteria counts (Escherichia coli, enterobacteraceae, Pseudomonas and enterococci) and the intestinal permeability, which was associated with the reduction of tight junctions and adherens junctions. Our results suggested that disruption of mucosal barrier and colonization resistance may be partly responsible for the bacterial translocation during chemotherapy. Thus, modulation of mechanical mucosal barrier and colonization resistance might represent a new opportunity for applications in cancer patients to reduce infectious complications.</description><subject>adherens junctions</subject><subject>Animals</subject><subject>Antineoplastic Agents - adverse effects</subject><subject>bacteria</subject><subject>Bacterial translocation</subject><subject>Cadherins - metabolism</subject><subject>chemotherapy</subject><subject>Cyclophosphamide</subject><subject>Cyclophosphamide - adverse effects</subject><subject>Enterococcus</subject><subject>Escherichia coli</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Intestinal microflora</subject><subject>intestinal microorganisms</subject><subject>Intestinal Mucosa - drug effects</subject><subject>Intestinal Mucosa - microbiology</subject><subject>Intestines - drug effects</subject><subject>Intestines - metabolism</subject><subject>Intestines - microbiology</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Microbiota - drug effects</subject><subject>Occludin - metabolism</subject><subject>patients</subject><subject>permeability</subject><subject>Permeability - drug effects</subject><subject>Pseudomonas</subject><subject>Tight junction</subject><subject>tight junctions</subject><subject>Zonula Occludens-1 Protein - metabolism</subject><issn>0014-2999</issn><issn>1879-0712</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kE1r3DAQhkVJaTZp_0FpfezFzow_ZOtSCKFNAoEcujmLkTTOavHHVtoN7L-vFqc5BgRCzDMzrx4hviIUCCivtgVvdxsKRQlYFSALAPlBrLBrVQ4tlmdiBYB1XiqlzsVFjFsAaFTZfBLnZdUqlIgrsV5vOLMbmp45Zn5yB8suM8fMHu0w7zZzTCtG7zjV0tlz3PuJhsxQCJ5DRpPLRm_D3A9zoBOUXvxZfOxpiPzl9b4UT79_rW_u8ofH2_ub64fcVp3c59gqVXJJnVEmZbMdulaRsQ22TSX73jkloXWgDNUdVtI5kgqMZUNGKqqqS_FjmbsL899DyqZHHy0PA008H6LGulSyRqybhNYLmrLGGLjXu-BHCkeNoE8-9VYvPvXJpwapk8_U9u11w8GM7N6a_gtMwPcF6GnW9Bx81E9_0oQmfajGpoZE_FwITiZekjQdrecpefaB7V672b-f4R9do5IQ</recordid><startdate>20130815</startdate><enddate>20130815</enddate><creator>Yang, Jin</creator><creator>Liu, Kai-xiong</creator><creator>Qu, Jie-ming</creator><creator>Wang, Xiao-dan</creator><general>Elsevier B.V</general><scope>FBQ</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>7X8</scope></search><sort><creationdate>20130815</creationdate><title>The changes induced by cyclophosphamide in intestinal barrier and microflora in mice</title><author>Yang, Jin ; Liu, Kai-xiong ; Qu, Jie-ming ; Wang, Xiao-dan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c386t-17992e2a8b9b000c81d79abc517536ffdd9607d09ba48136dda690bcebab69a33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>adherens junctions</topic><topic>Animals</topic><topic>Antineoplastic Agents - adverse effects</topic><topic>bacteria</topic><topic>Bacterial translocation</topic><topic>Cadherins - metabolism</topic><topic>chemotherapy</topic><topic>Cyclophosphamide</topic><topic>Cyclophosphamide - adverse effects</topic><topic>Enterococcus</topic><topic>Escherichia coli</topic><topic>Gene Expression Regulation - drug effects</topic><topic>Intestinal microflora</topic><topic>intestinal microorganisms</topic><topic>Intestinal Mucosa - drug effects</topic><topic>Intestinal Mucosa - microbiology</topic><topic>Intestines - drug effects</topic><topic>Intestines - metabolism</topic><topic>Intestines - microbiology</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Microbiota - drug effects</topic><topic>Occludin - metabolism</topic><topic>patients</topic><topic>permeability</topic><topic>Permeability - drug effects</topic><topic>Pseudomonas</topic><topic>Tight junction</topic><topic>tight junctions</topic><topic>Zonula Occludens-1 Protein - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yang, Jin</creatorcontrib><creatorcontrib>Liu, Kai-xiong</creatorcontrib><creatorcontrib>Qu, Jie-ming</creatorcontrib><creatorcontrib>Wang, Xiao-dan</creatorcontrib><collection>AGRIS</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>European journal of pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yang, Jin</au><au>Liu, Kai-xiong</au><au>Qu, Jie-ming</au><au>Wang, Xiao-dan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The changes induced by cyclophosphamide in intestinal barrier and microflora in mice</atitle><jtitle>European journal of pharmacology</jtitle><addtitle>Eur J Pharmacol</addtitle><date>2013-08-15</date><risdate>2013</risdate><volume>714</volume><issue>1-3</issue><spage>120</spage><epage>124</epage><pages>120-124</pages><issn>0014-2999</issn><eissn>1879-0712</eissn><abstract>Infection is one of the most commonly encountered complication during chemotherapy treatment, and recent studies showed that such infections are aroused primarily from the intestinal microflora through bacterial translocation. We aimed to investigate the alterations of mucosal barrier and colonization resistance in mouse treated with cyclophosphamide (CTX) to further understand the translocation mechanism. Male Balb/c mice were administered intraperitoneally with CTX at 25mg/kg, 50mg/kg and 100mg/kg for 5 days. We found that pretreatment with CTX, especially at high dose, increased the potentially pathogenic bacteria counts (Escherichia coli, enterobacteraceae, Pseudomonas and enterococci) and the intestinal permeability, which was associated with the reduction of tight junctions and adherens junctions. Our results suggested that disruption of mucosal barrier and colonization resistance may be partly responsible for the bacterial translocation during chemotherapy. Thus, modulation of mechanical mucosal barrier and colonization resistance might represent a new opportunity for applications in cancer patients to reduce infectious complications.</abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>23791611</pmid><doi>10.1016/j.ejphar.2013.06.006</doi><tpages>5</tpages></addata></record> |
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| source | MEDLINE; Elsevier ScienceDirect Journals Complete |
| subjects | adherens junctions Animals Antineoplastic Agents - adverse effects bacteria Bacterial translocation Cadherins - metabolism chemotherapy Cyclophosphamide Cyclophosphamide - adverse effects Enterococcus Escherichia coli Gene Expression Regulation - drug effects Intestinal microflora intestinal microorganisms Intestinal Mucosa - drug effects Intestinal Mucosa - microbiology Intestines - drug effects Intestines - metabolism Intestines - microbiology Male Mice Mice, Inbred BALB C Microbiota - drug effects Occludin - metabolism patients permeability Permeability - drug effects Pseudomonas Tight junction tight junctions Zonula Occludens-1 Protein - metabolism |
| title | The changes induced by cyclophosphamide in intestinal barrier and microflora in mice |
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