Anti-inflammatory consequences of bile acid accumulation in virus-infected bile duct ligated mice
Cholestatic patients exhibiting high bile acid serum levels were reported to be more susceptible to bacterial and viral infections. Animal studies in bile duct ligated (BDL) mice suggest that cholestasis leads to an aggravation of hepatic bacterial infections. We have investigated the impact of chol...
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| creator | Rattay, Stephanie Graf, Dirk Kislat, Andreas Homey, Bernhard Herebian, Diran Häussinger, Dieter Hengel, Hartmut Zimmermann, Albert Schupp, Anna-Kathrin |
| description | Cholestatic patients exhibiting high bile acid serum levels were reported to be more susceptible to bacterial and viral infections. Animal studies in bile duct ligated (BDL) mice suggest that cholestasis leads to an aggravation of hepatic bacterial infections. We have investigated the impact of cholestasis on mouse cytomegalovirus (MCMV)-induced immune responses and viral replication. While MCMV did not aggravate BDL-induced liver damage, BDL markedly reduced MCMV-triggered chemokine expression and immune cell recruitment to the liver. MCMV-infected BDL mice showed diminished trafficking of Ly6C+/F4/80+ myeloid cells and NK1.1+ NK cells to the liver compared to MCMV infected control mice. Moreover, virus-driven expression of CCL7, CCL12, CXCL9 and CXCL10 was clearly impaired in BDL- compared to sham-operated mice. Furthermore, production of the anti-inflammatory cytokine IL-10 was massively augmented in infected BDL mice. In contrast, intra- and extrahepatic virus replication was unaltered in BDL-MCMV mice when compared to sham-MCMV mice. Cholestasis in the BDL model severely impaired pathogen-induced chemokine expression in the liver affecting CCR2- and CXCR3-dependent cell trafficking. Cholestasis resulted in reduced recruitment of inflammatory monocytes and NK cells to the liver. |
| doi_str_mv | 10.1371/journal.pone.0199863 |
| format | Article |
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Animal studies in bile duct ligated (BDL) mice suggest that cholestasis leads to an aggravation of hepatic bacterial infections. We have investigated the impact of cholestasis on mouse cytomegalovirus (MCMV)-induced immune responses and viral replication. While MCMV did not aggravate BDL-induced liver damage, BDL markedly reduced MCMV-triggered chemokine expression and immune cell recruitment to the liver. MCMV-infected BDL mice showed diminished trafficking of Ly6C+/F4/80+ myeloid cells and NK1.1+ NK cells to the liver compared to MCMV infected control mice. Moreover, virus-driven expression of CCL7, CCL12, CXCL9 and CXCL10 was clearly impaired in BDL- compared to sham-operated mice. Furthermore, production of the anti-inflammatory cytokine IL-10 was massively augmented in infected BDL mice. In contrast, intra- and extrahepatic virus replication was unaltered in BDL-MCMV mice when compared to sham-MCMV mice. Cholestasis in the BDL model severely impaired pathogen-induced chemokine expression in the liver affecting CCR2- and CXCR3-dependent cell trafficking. Cholestasis resulted in reduced recruitment of inflammatory monocytes and NK cells to the liver.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0199863</identifier><identifier>PMID: 29953538</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Acids ; Bile ; Bile acids ; Bile ducts ; Biology and Life Sciences ; Care and treatment ; CCR2 protein ; Cholestasis ; CXCL10 protein ; CXCR3 protein ; Cytomegalovirus ; Cytomegalovirus infections ; Development and progression ; Health aspects ; Hepatocytes ; Immune response ; Infections ; Inflammation ; Influence ; Interleukin 10 ; Liver ; Medicine and Health Sciences ; Mice ; Monocyte chemoattractant protein 1 ; Monocytes ; Mortality ; Myeloid cells ; Physiological aspects ; Replication ; Rodents ; Serum levels ; Viruses</subject><ispartof>PloS one, 2018-06, Vol.13 (6), p.e0199863-e0199863</ispartof><rights>COPYRIGHT 2018 Public Library of Science</rights><rights>2018 Rattay et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2018 Rattay et al 2018 Rattay et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c692t-d072c90e4f1a81647f0ee9ec47dc9ea2e36480ce59cfed3fbcde06993a1802013</citedby><cites>FETCH-LOGICAL-c692t-d072c90e4f1a81647f0ee9ec47dc9ea2e36480ce59cfed3fbcde06993a1802013</cites><orcidid>0000-0002-0273-7992</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/PMC6023182/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6023182/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79342,79343</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29953538$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Rattay, Stephanie</creatorcontrib><creatorcontrib>Graf, Dirk</creatorcontrib><creatorcontrib>Kislat, Andreas</creatorcontrib><creatorcontrib>Homey, Bernhard</creatorcontrib><creatorcontrib>Herebian, Diran</creatorcontrib><creatorcontrib>Häussinger, Dieter</creatorcontrib><creatorcontrib>Hengel, Hartmut</creatorcontrib><creatorcontrib>Zimmermann, Albert</creatorcontrib><creatorcontrib>Schupp, Anna-Kathrin</creatorcontrib><title>Anti-inflammatory consequences of bile acid accumulation in virus-infected bile duct ligated mice</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Cholestatic patients exhibiting high bile acid serum levels were reported to be more susceptible to bacterial and viral infections. Animal studies in bile duct ligated (BDL) mice suggest that cholestasis leads to an aggravation of hepatic bacterial infections. We have investigated the impact of cholestasis on mouse cytomegalovirus (MCMV)-induced immune responses and viral replication. While MCMV did not aggravate BDL-induced liver damage, BDL markedly reduced MCMV-triggered chemokine expression and immune cell recruitment to the liver. MCMV-infected BDL mice showed diminished trafficking of Ly6C+/F4/80+ myeloid cells and NK1.1+ NK cells to the liver compared to MCMV infected control mice. Moreover, virus-driven expression of CCL7, CCL12, CXCL9 and CXCL10 was clearly impaired in BDL- compared to sham-operated mice. Furthermore, production of the anti-inflammatory cytokine IL-10 was massively augmented in infected BDL mice. In contrast, intra- and extrahepatic virus replication was unaltered in BDL-MCMV mice when compared to sham-MCMV mice. Cholestasis in the BDL model severely impaired pathogen-induced chemokine expression in the liver affecting CCR2- and CXCR3-dependent cell trafficking. Cholestasis resulted in reduced recruitment of inflammatory monocytes and NK cells to the liver.</description><subject>Acids</subject><subject>Bile</subject><subject>Bile acids</subject><subject>Bile ducts</subject><subject>Biology and Life Sciences</subject><subject>Care and treatment</subject><subject>CCR2 protein</subject><subject>Cholestasis</subject><subject>CXCL10 protein</subject><subject>CXCR3 protein</subject><subject>Cytomegalovirus</subject><subject>Cytomegalovirus infections</subject><subject>Development and progression</subject><subject>Health aspects</subject><subject>Hepatocytes</subject><subject>Immune response</subject><subject>Infections</subject><subject>Inflammation</subject><subject>Influence</subject><subject>Interleukin 10</subject><subject>Liver</subject><subject>Medicine and Health Sciences</subject><subject>Mice</subject><subject>Monocyte chemoattractant protein 1</subject><subject>Monocytes</subject><subject>Mortality</subject><subject>Myeloid 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Anna-Kathrin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Anti-inflammatory consequences of bile acid accumulation in virus-infected bile duct ligated mice</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2018-06-28</date><risdate>2018</risdate><volume>13</volume><issue>6</issue><spage>e0199863</spage><epage>e0199863</epage><pages>e0199863-e0199863</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Cholestatic patients exhibiting high bile acid serum levels were reported to be more susceptible to bacterial and viral infections. Animal studies in bile duct ligated (BDL) mice suggest that cholestasis leads to an aggravation of hepatic bacterial infections. We have investigated the impact of cholestasis on mouse cytomegalovirus (MCMV)-induced immune responses and viral replication. While MCMV did not aggravate BDL-induced liver damage, BDL markedly reduced MCMV-triggered chemokine expression and immune cell recruitment to the liver. MCMV-infected BDL mice showed diminished trafficking of Ly6C+/F4/80+ myeloid cells and NK1.1+ NK cells to the liver compared to MCMV infected control mice. Moreover, virus-driven expression of CCL7, CCL12, CXCL9 and CXCL10 was clearly impaired in BDL- compared to sham-operated mice. Furthermore, production of the anti-inflammatory cytokine IL-10 was massively augmented in infected BDL mice. In contrast, intra- and extrahepatic virus replication was unaltered in BDL-MCMV mice when compared to sham-MCMV mice. Cholestasis in the BDL model severely impaired pathogen-induced chemokine expression in the liver affecting CCR2- and CXCR3-dependent cell trafficking. Cholestasis resulted in reduced recruitment of inflammatory monocytes and NK cells to the liver.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>29953538</pmid><doi>10.1371/journal.pone.0199863</doi><tpages>e0199863</tpages><orcidid>https://orcid.org/0000-0002-0273-7992</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Acids Bile Bile acids Bile ducts Biology and Life Sciences Care and treatment CCR2 protein Cholestasis CXCL10 protein CXCR3 protein Cytomegalovirus Cytomegalovirus infections Development and progression Health aspects Hepatocytes Immune response Infections Inflammation Influence Interleukin 10 Liver Medicine and Health Sciences Mice Monocyte chemoattractant protein 1 Monocytes Mortality Myeloid cells Physiological aspects Replication Rodents Serum levels Viruses |
| title | Anti-inflammatory consequences of bile acid accumulation in virus-infected bile duct ligated mice |
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