FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2169587716> ?p ?o ?g. }

• W2169587716 endingPage "4817" @default.
• W2169587716 startingPage "4809" @default.
• W2169587716 abstract "ABSTRACT Due to a scarcity of immunocompetent animal models for viral hepatitis, little is known about the early innate immune responses in the liver. In various hepatotoxic models, both pro- and anti-inflammatory activities of recruited monocytes have been described. In this study, we compared the effect of liver inflammation induced by the Toll-like receptor 4 ligand lipopolysaccharide (LPS) with that of a persistent virus, lymphocytic choriomeningitis virus (LCMV) clone 13, on early innate intrahepatic immune responses in mice. LCMV infection induces a remarkable influx of inflammatory monocytes in the liver within 24 h, accompanied by increased transcript levels of several proinflammatory cytokines and chemokines in whole liver. Importantly, while a single LPS injection results in similar recruitment of inflammatory monocytes to the liver, the functional properties of the infiltrating cells are dramatically different in response to LPS versus LCMV infection. In fact, intrahepatic inflammatory monocytes are skewed toward a secretory phenotype with impaired phagocytosis in LCMV-induced liver inflammation but exhibit increased endocytic capacity after LPS challenge. In contrast, F4/80 high -Kupffer cells retain their steady-state endocytic functions upon LCMV infection. Strikingly, the gene expression levels of inflammatory monocytes dramatically change upon LCMV exposure and resemble those of Kupffer cells. Since inflammatory monocytes outnumber Kupffer cells 24 h after LCMV infection, it is highly likely that inflammatory monocytes contribute to the intrahepatic inflammatory response during the early phase of infection. Our findings are instrumental in understanding the early immunological events during virus-induced liver disease and point toward inflammatory monocytes as potential target cells for future treatment options in viral hepatitis. IMPORTANCE Insights into how the immune system deals with hepatitis B virus (HBV) and HCV are scarce due to the lack of adequate animal model systems. This knowledge is, however, crucial to developing new antiviral strategies aimed at eradicating these chronic infections. We model virus-host interactions during the initial phase of liver inflammation 24 h after inoculating mice with LCMV. We show that infected Kupffer cells are rapidly outnumbered by infiltrating inflammatory monocytes, which secrete proinflammatory cytokines but are less phagocytic. Nevertheless, these recruited inflammatory monocytes start to resemble Kupffer cells on a transcript level. The specificity of these cellular changes for virus-induced liver inflammation is corroborated by demonstrating opposite functions of monocytes after LPS challenge. Overall, this demonstrates the enormous functional and genetic plasticity of infiltrating monocytes and identifies them as an important target cell for future treatment regimens." @default.
• W2169587716 created "2016-06-24" @default.
• W2169587716 creator A5000852072 @default.
• W2169587716 creator A5004691327 @default.
• W2169587716 creator A5024630515 @default.
• W2169587716 creator A5030434932 @default.
• W2169587716 creator A5040277974 @default.
• W2169587716 creator A5042260251 @default.
• W2169587716 creator A5043626370 @default.
• W2169587716 creator A5061113823 @default.
• W2169587716 creator A5067136189 @default.
• W2169587716 creator A5073298216 @default.
• W2169587716 creator A5082050840 @default.
• W2169587716 creator A5090542795 @default.
• W2169587716 date "2015-05-01" @default.
• W2169587716 modified "2023-10-17" @default.
• W2169587716 title "Inflammatory Monocytes Recruited to the Liver within 24 Hours after Virus-Induced Inflammation Resemble Kupffer Cells but Are Functionally Distinct" @default.
• W2169587716 cites W1491184522 @default.
• W2169587716 cites W1511703016 @default.
• W2169587716 cites W1545441058 @default.
• W2169587716 cites W1941945396 @default.
• W2169587716 cites W1966848960 @default.
• W2169587716 cites W1969361825 @default.
• W2169587716 cites W1977142289 @default.
• W2169587716 cites W1979292513 @default.
• W2169587716 cites W1983585538 @default.
• W2169587716 cites W1987344938 @default.
• W2169587716 cites W1990083653 @default.
• W2169587716 cites W1992114061 @default.
• W2169587716 cites W1992603628 @default.
• W2169587716 cites W2003616999 @default.
• W2169587716 cites W2018286119 @default.
• W2169587716 cites W2029129294 @default.
• W2169587716 cites W2033304214 @default.
• W2169587716 cites W2034598453 @default.
• W2169587716 cites W2037933015 @default.
• W2169587716 cites W2044951291 @default.
• W2169587716 cites W2048134603 @default.
• W2169587716 cites W2048511851 @default.
• W2169587716 cites W2049247030 @default.
• W2169587716 cites W2056331787 @default.
• W2169587716 cites W2071267501 @default.
• W2169587716 cites W2083872083 @default.
• W2169587716 cites W2085099489 @default.
• W2169587716 cites W2110456507 @default.
• W2169587716 cites W2111253543 @default.
• W2169587716 cites W2111550054 @default.
• W2169587716 cites W2111718223 @default.
• W2169587716 cites W2113525720 @default.
• W2169587716 cites W2119569986 @default.
• W2169587716 cites W2121592233 @default.
• W2169587716 cites W2130259551 @default.
• W2169587716 cites W2145534694 @default.
• W2169587716 cites W2150364184 @default.
• W2169587716 cites W2150695445 @default.
• W2169587716 cites W2150781849 @default.
• W2169587716 cites W2151586546 @default.
• W2169587716 cites W2152909181 @default.
• W2169587716 cites W2152923082 @default.
• W2169587716 cites W2159337363 @default.
• W2169587716 cites W2160142989 @default.
• W2169587716 cites W2164563425 @default.
• W2169587716 cites W2169135788 @default.
• W2169587716 cites W2333452860 @default.
• W2169587716 cites W2394604721 @default.
• W2169587716 doi "https://doi.org/10.1128/jvi.03733-14" @default.
• W2169587716 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4403491" @default.
• W2169587716 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/25673700" @default.
• W2169587716 hasPublicationYear "2015" @default.
• W2169587716 type Work @default.
• W2169587716 sameAs 2169587716 @default.
• W2169587716 citedByCount "35" @default.
• W2169587716 countsByYear W21695877162016 @default.
• W2169587716 countsByYear W21695877162017 @default.
• W2169587716 countsByYear W21695877162018 @default.
• W2169587716 countsByYear W21695877162019 @default.
• W2169587716 countsByYear W21695877162020 @default.
• W2169587716 countsByYear W21695877162021 @default.
• W2169587716 countsByYear W21695877162022 @default.
• W2169587716 crossrefType "journal-article" @default.
• W2169587716 hasAuthorship W2169587716A5000852072 @default.
• W2169587716 hasAuthorship W2169587716A5004691327 @default.
• W2169587716 hasAuthorship W2169587716A5024630515 @default.
• W2169587716 hasAuthorship W2169587716A5030434932 @default.
• W2169587716 hasAuthorship W2169587716A5040277974 @default.
• W2169587716 hasAuthorship W2169587716A5042260251 @default.
• W2169587716 hasAuthorship W2169587716A5043626370 @default.
• W2169587716 hasAuthorship W2169587716A5061113823 @default.
• W2169587716 hasAuthorship W2169587716A5067136189 @default.
• W2169587716 hasAuthorship W2169587716A5073298216 @default.
• W2169587716 hasAuthorship W2169587716A5082050840 @default.
• W2169587716 hasAuthorship W2169587716A5090542795 @default.
• W2169587716 hasBestOaLocation W21695877161 @default.
• W2169587716 hasConcept C13373296 @default.
• W2169587716 hasConcept C136449434 @default.
• W2169587716 hasConcept C164027704 @default.
• W2169587716 hasConcept C167672396 @default.
• W2169587716 hasConcept C203014093 @default.

• next