About: Macrophage activation state determines the response to rhinovirus infection in a mouse model of allergic asthma

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About: Macrophage activation state determines the response to rhinovirus infection in a mouse model of allergic asthma Goto Sponge NotDistinct Permalink

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type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Macrophage activation state determines the response to rhinovirus infection in a mouse model of allergic asthma
Creator	Chen, Qiang Lei, Jing Chung, Yutein Steenrod, Jessica Comstock, Adam Goldsmith, Adam Hershenson, Marc Sajjan, Uma Kelley Bentley, J Young, Jun
Source	Medline; PMC
abstract	BACKGROUND: The mechanisms by which viruses cause asthma exacerbations are not precisely known. Previously, we showed that, in ovalbumin (OVA)-sensitized and -challenged mice with allergic airway inflammation, rhinovirus (RV) infection increases type 2 cytokine production from alternatively-activated (M2) airway macrophages, enhancing eosinophilic inflammation and airways hyperresponsiveness. In this paper, we tested the hypothesis that IL-4 signaling determines the state of macrophage activation and pattern of RV-induced exacerbation in mice with allergic airways disease. METHODS: Eight week-old wild type or IL-4 receptor knockout (IL-4R KO) mice were sensitized and challenged with OVA and inoculated with RV1B or sham HeLa cell lysate. RESULTS: In contrast to OVA-treated wild-type mice with both neutrophilic and eosinophilic airway inflammation, OVA-treated IL-4R KO mice showed increased neutrophilic inflammation with few eosinophils in the airways. Like wild-type mice, IL-4R KO mice showed OVA-induced airway hyperreactivity which was further exacerbated by RV. There was a shift in lung cytokines from a type 2-predominant response to a type 1 response, including production of IL-12p40 and TNF-α. IL-17A was also increased. RV infection of OVA-treated IL-4R KO mice further increased neutrophilic inflammation. Bronchoalveolar macrophages showed an M1 polarization pattern and ex vivo RV infection increased macrophage production of TNF-α, IFN-γ and IL-12p40. Finally, lung cells from OVA-treated IL-4R KO mice showed reduced CD206+ CD301+ M2 macrophages, decreased IL-13 and increased TNF-α and IL-17A production by F4/80+, CD11b+ macrophages. CONCLUSIONS: OVA-treated IL-4R KO mice show neutrophilic airway inflammation constituting a model of allergic, type 1 cytokine-driven neutrophilic asthma. In the absence of IL-4/IL-13 signaling, RV infection of OVA-treated mice increased type 1 cytokine and IL-17A production from conventionally-activated macrophages, augmenting neutrophilic rather than eosinophilic inflammation. In mice with allergic airways inflammation, IL-4R signaling determines macrophage activation state and the response to subsequent RV infection.
has issue date	2014-06-07(xsd:dateTime)
bibo:doi	10.1186/1465-9921-15-63
bibo:pmid	24907978
has license	cc-by
sha1sum (hex)	c12642f0762cb4888b417ce295044080ab9202a6
schema:url	https://doi.org/10.1186/1465-9921-15-63
resource representing a document's title	Macrophage activation state determines the response to rhinovirus infection in a mouse model of allergic asthma
has PubMed Central identifier	PMC4066837
has PubMed identifier	24907978
schema:publication	Respir Res
resource representing a document's body	covid:c12642f0762cb4888b417ce295044080ab9202a6#body_text
is schema:about of	named entity 'CELLS' named entity 'METHODS' named entity 'WILD TYPE' named entity 'ABSENCE OF' named entity 'STATE' named entity 'PRODUCTION' named entity 'CELL LYSATE' named entity 'CAUSE' named entity 'DECREASED' named entity 'AIRWAYS DISEASE' named entity 'INDUCED' named entity 'INCREASES' named entity 'IL-13' named entity 'PREVIOUSLY' named entity 'EOSINOPHILS' named entity 'LUNG' named entity 'HYPOTHESIS' named entity 'TYPE 2' named entity 'ACTIVATED' named entity 'RESPONSE' named entity 'RATHER' named entity 'EXACERBATION' named entity 'PATTERN' named entity 'TNF' named entity 'IL-4' named entity 'A TYPE 2' named entity 'CD11b+' named entity 'IL-12p40' named entity 'determines' named entity 'wild-type' named entity 'production' named entity 'macrophages' named entity 'activation' named entity 'MODEL OF' named entity 'RESPONSE TO' named entity 'PREDOMINANT' named entity 'IL-4 RECEPTOR' named entity 'REDUCED' named entity 'MACROPHAGES' named entity 'ALLERGIC' named entity 'AIRWAY' named entity 'MECHANISMS' named entity 'MICE' named entity 'CONTRAST' named entity 'MACROPHAGE ACTIVATION' named entity 'OLD' named entity 'EOSINOPHILIC AIRWAY INFLAMMATION' named entity 'WAS A' named entity 'ENHANCING' named entity 'TYPE 1' named entity 'TREATED' named entity 'CD206' named entity 'INCLUDING' named entity 'IL-17A PRODUCTION' named entity 'NEUTROPHILIC' named entity 'CYTOKINE PRODUCTION' named entity 'OVA' named entity 'AIRWAY HYPERREACTIVITY' named entity 'PAPER' named entity 'IFN' named entity 'TESTED' named entity 'CD301' named entity 'EX VIVO' named entity 'MOUSE MODEL' named entity 'A MOUSE' named entity 'ALLERGIC ASTHMA' named entity 'NEUTROPHILIC AIRWAY INFLAMMATION' named entity 'IL-12P40' named entity 'RESPONSE TO' named entity 'EXACERBATED BY' named entity 'INFECTION' named entity 'SIGNALING'

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