FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2005172029> ?p ?o ?g. }

• W2005172029 endingPage "9567" @default.
• W2005172029 startingPage "9553" @default.
• W2005172029 abstract "ABSTRACT The encephalitic response to viral infection requires local chemokine production and the ensuing recruitment of immune and inflammatory leukocytes. Accordingly, chemokine receptors present themselves as plausible therapeutic targets for drugs aimed at limiting encephalitic responses. However, it remains unclear which chemokines are central to this process and whether leukocyte recruitment is important for limiting viral proliferation and survival in the brain or whether it is predominantly a driver of coincident inflammatory pathogenesis. Here we examine chemokine expression and leukocyte recruitment in the context of avirulent and virulent Semliki Forest virus (SFV) as well as West Nile virus infection and demonstrate rapid and robust expression of a variety of inflammatory CC and CXC chemokines in all models. On this basis, we define a chemokine axis involved in leukocyte recruitment to the encephalitic brain during SFV infection. CXCR3 is the most active; CCR2 is also active but less so, and CCR5 plays only a modest role in leukocyte recruitment. Importantly, inhibition of each of these receptors individually and the resulting suppression of leukocyte recruitment to the infected brain have no effect on viral titer or survival following infection with a virulent SFV strain. In contrast, simultaneous blockade of CXCR3 and CCR2 results in significantly reduced mortality in response to virulent SFV infection. In summary, therefore, our data provide an unprecedented level of insight into chemokine orchestration of leukocyte recruitment in viral encephalitis. Our data also highlight CXCR3 and CCR2 as possible therapeutic targets for limiting inflammatory damage in response to viral infection of the brain. IMPORTANCE Brain inflammation (encephalitis) in response to viral infection can lead to severe illness and even death. This therefore represents an important clinical problem and one that requires the development of new therapeutic approaches. Central to the pathogenesis of encephalitis is the recruitment of inflammatory leukocytes to the infected brain, a process driven by members of the chemokine family. Here we provide an in-depth analysis of the chemokines involved in leukocyte recruitment to the virally infected brain and demonstrate that simultaneous blockade of two of these receptors, namely, CXCR3 and CCR2, does not alter viral titers within the brain but markedly reduces inflammatory leukocyte recruitment and enhances survival in a murine model of lethal viral encephalitis. Our results therefore highlight chemokine receptors as plausible therapeutic targets in treating viral encephalitis." @default.
• W2005172029 created "2016-06-24" @default.
• W2005172029 creator A5004327792 @default.
• W2005172029 creator A5017958130 @default.
• W2005172029 creator A5027149692 @default.
• W2005172029 creator A5027463016 @default.
• W2005172029 creator A5040423570 @default.
• W2005172029 creator A5056001873 @default.
• W2005172029 creator A5074696946 @default.
• W2005172029 creator A5077150652 @default.
• W2005172029 date "2014-09-01" @default.
• W2005172029 modified "2023-09-27" @default.
• W2005172029 title "Defining the Chemokine Basis for Leukocyte Recruitment during Viral Encephalitis" @default.
• W2005172029 cites W1555404884 @default.
• W2005172029 cites W1582143860 @default.
• W2005172029 cites W1600316672 @default.
• W2005172029 cites W1818847823 @default.
• W2005172029 cites W1922705469 @default.
• W2005172029 cites W1970049876 @default.
• W2005172029 cites W1974367364 @default.
• W2005172029 cites W1976838885 @default.
• W2005172029 cites W1978201079 @default.
• W2005172029 cites W1980307352 @default.
• W2005172029 cites W1987332793 @default.
• W2005172029 cites W2001092796 @default.
• W2005172029 cites W2002489008 @default.
• W2005172029 cites W2002668555 @default.
• W2005172029 cites W2009998721 @default.
• W2005172029 cites W2026578487 @default.
• W2005172029 cites W2038768395 @default.
• W2005172029 cites W2039008625 @default.
• W2005172029 cites W2039943918 @default.
• W2005172029 cites W2040383994 @default.
• W2005172029 cites W2046770212 @default.
• W2005172029 cites W2046905438 @default.
• W2005172029 cites W2047225513 @default.
• W2005172029 cites W2055972388 @default.
• W2005172029 cites W2056967541 @default.
• W2005172029 cites W2058189238 @default.
• W2005172029 cites W2060279158 @default.
• W2005172029 cites W2065142998 @default.
• W2005172029 cites W2066514302 @default.
• W2005172029 cites W2069149379 @default.
• W2005172029 cites W2080127227 @default.
• W2005172029 cites W2084121962 @default.
• W2005172029 cites W2088301466 @default.
• W2005172029 cites W2091648107 @default.
• W2005172029 cites W2095767844 @default.
• W2005172029 cites W2098058601 @default.
• W2005172029 cites W2102947626 @default.
• W2005172029 cites W2104003768 @default.
• W2005172029 cites W2108971625 @default.
• W2005172029 cites W2111800376 @default.
• W2005172029 cites W2114570899 @default.
• W2005172029 cites W2117711297 @default.
• W2005172029 cites W2118128317 @default.
• W2005172029 cites W2120454824 @default.
• W2005172029 cites W2120996101 @default.
• W2005172029 cites W2127395567 @default.
• W2005172029 cites W2136716619 @default.
• W2005172029 cites W2138780833 @default.
• W2005172029 cites W2141410012 @default.
• W2005172029 cites W2142792546 @default.
• W2005172029 cites W2142913420 @default.
• W2005172029 cites W2147169218 @default.
• W2005172029 cites W2148740102 @default.
• W2005172029 cites W2148769634 @default.
• W2005172029 cites W2149787553 @default.
• W2005172029 cites W2152094131 @default.
• W2005172029 cites W2155589041 @default.
• W2005172029 cites W2167525669 @default.
• W2005172029 cites W4248838553 @default.
• W2005172029 cites W97158386 @default.
• W2005172029 doi "https://doi.org/10.1128/jvi.03421-13" @default.
• W2005172029 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4136330" @default.
• W2005172029 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/24899190" @default.
• W2005172029 hasPublicationYear "2014" @default.
• W2005172029 type Work @default.
• W2005172029 sameAs 2005172029 @default.
• W2005172029 citedByCount "40" @default.
• W2005172029 countsByYear W20051720292015 @default.
• W2005172029 countsByYear W20051720292016 @default.
• W2005172029 countsByYear W20051720292017 @default.
• W2005172029 countsByYear W20051720292018 @default.
• W2005172029 countsByYear W20051720292019 @default.
• W2005172029 countsByYear W20051720292020 @default.
• W2005172029 countsByYear W20051720292021 @default.
• W2005172029 countsByYear W20051720292022 @default.
• W2005172029 countsByYear W20051720292023 @default.
• W2005172029 crossrefType "journal-article" @default.
• W2005172029 hasAuthorship W2005172029A5004327792 @default.
• W2005172029 hasAuthorship W2005172029A5017958130 @default.
• W2005172029 hasAuthorship W2005172029A5027149692 @default.
• W2005172029 hasAuthorship W2005172029A5027463016 @default.
• W2005172029 hasAuthorship W2005172029A5040423570 @default.
• W2005172029 hasAuthorship W2005172029A5056001873 @default.
• W2005172029 hasAuthorship W2005172029A5074696946 @default.
• W2005172029 hasAuthorship W2005172029A5077150652 @default.

• next