About: IL-4/IL-13 polarization of macrophages enhances Ebola virus glycoprotein-dependent infection

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About: IL-4/IL-13 polarization of macrophages enhances Ebola virus glycoprotein-dependent infection Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : covidontheweb.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	IL-4/IL-13 polarization of macrophages enhances Ebola virus glycoprotein-dependent infection
Creator	Chen, Jing Brunton, Bethany Rogers, Kai Bohan, Dana Mallinger, Laura Mauryid, Wendy Sevcik, Kristina Ruggioid, Natalie
Source	PMC
abstract	BACKGROUND: Ebolavirus (EBOV) outbreaks, while sporadic, cause tremendous morbidity and mortality. No therapeutics or vaccines are currently licensed; however, a vaccine has shown promise in clinical trials. A critical step towards development of effective therapeutics is a better understanding of factors that govern host susceptibility to this pathogen. As macrophages are an important cell population targeted during virus replication, we explore the effect of cytokine polarization on macrophage infection. METHODS/MAIN FINDINGS: We utilized a BSL2 EBOV model virus, infectious, recombinant vesicular stomatitis virus encoding EBOV glycoprotein (GP) (rVSV/EBOV GP) in place of its native glycoprotein. Macrophages polarized towards a M2-like anti-inflammatory state by combined IL-4 and IL-13 treatment were more susceptible to rVSV/EBOV GP, but not to wild-type VSV (rVSV/G), suggesting that EBOV GP-dependent entry events were enhanced by these cytokines. Examination of RNA expression of known surface receptors that bind and internalize filoviruses demonstrated that IL-4/IL-13 stimulated expression of the C-type lectin receptor DC-SIGN in human macrophages and addition of the competitive inhibitor mannan abrogated IL-4/IL-13 enhanced infection. Two murine DC-SIGN-like family members, SIGNR3 and SIGNR5, were upregulated by IL-4/IL-13 in murine macrophages, but only SIGNR3 enhanced virus infection in a mannan-inhibited manner, suggesting that murine SIGNR3 plays a similar role to human DC-SIGN. In vivo IL-4/IL-13 administration significantly increased virus-mediated mortality in a mouse model and transfer of ex vivo IL-4/IL-13-treated murine peritoneal macrophages into the peritoneal cavity of mice enhanced pathogenesis. SIGNIFICANCE: These studies highlight the ability of macrophage polarization to influence EBOV GP-dependent virus replication in vivo and ex vivo, with M2a polarization upregulating cell surface receptor expression and thereby enhancing virus replication. Our findings provide an increased understanding of the host factors in macrophages governing susceptibility to filoviruses and identify novel murine receptors mediating EBOV entry.
has issue date	2019-12-11(xsd:dateTime)
bibo:doi	10.1371/journal.pntd.0007819
bibo:pmid	31825972
has license	cc-by
sha1sum (hex)	29e94dee0df31f591c6f09c590e4c3523a14e647
schema:url	https://doi.org/10.1371/journal.pntd.0007819
resource representing a document's title	IL-4/IL-13 polarization of macrophages enhances Ebola virus glycoprotein-dependent infection
has PubMed Central identifier	PMC6905523
has PubMed identifier	31825972
schema:publication	PLoS Negl Trop Dis
resource representing a document's body	covid:29e94dee0df31f591c6f09c590e4c3523a14e647#body_text
is schema:about of	named entity 'development' named entity 'vaccine' named entity 'mortality' covid:arg/29e94dee0df31f591c6f09c590e4c3523a14e647 named entity 'population' named entity 'polarization' named entity 'EBOV' named entity 'IL-13' named entity 'Ebola virus' named entity 'promise' named entity 'TLR4' named entity 'glycoprotein' named entity 'macrophage polarization' named entity 'cell surface receptors' named entity 'CLRs' named entity 'IACUC' named entity 'HIV-1' named entity 'DC-SIGN' named entity 'IL-4' named entity 'IL-4' named entity 'TIM-4' named entity 'EBOV' named entity 'roundworm' named entity 'TIM-4' named entity 'cytokines' named entity 'IL-13' named entity 'viral pathogenesis' named entity 'endosomal' named entity 'virus like particle' named entity 'cytokines' named entity 'IL-4' named entity 'filovirus' named entity 'M2a' named entity 'IL-12' named entity 'Ifnar' named entity 'VLP' named entity 'cytokine' named entity 'macrophages' named entity 'IL-4' named entity 'Ifnar' named entity 'IL-10' named entity 'anesthetized' named entity 'wild-type' named entity 'breeding colony' named entity 'EBOV' named entity 'phenotypically' named entity 'macrophage' named entity 'Brucella' named entity 'IL-13' named entity 'HIV-1 and HIV-2' named entity 'VP40' named entity 'macrophages' named entity 'National Institutes of Health' named entity 'Ifnar' named entity 'nonspecific symptoms' named entity 'plasmid DNA' named entity 'IL-4' named entity 'HEK 293T' named entity 'filovirus' named entity 'infection' named entity 'IL-4' named entity 'TRIzol' named entity 'left ventricle' named entity 'macrophages' named entity 'EBOV' named entity 'filovirus' named entity 'liposomes' named entity 'IL-13' named entity 'infection' named entity 'standard deviation' named entity 'Leishmania' named entity 'proinflammatory' named entity 'DC-SIGN' named entity 'DC-SIGN'

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