FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2140709510> ?p ?o ?g. }

• W2140709510 endingPage "1438.e7" @default.
• W2140709510 startingPage "1429" @default.
• W2140709510 abstract "BackgroundAllergic asthma is a chronic disease of the conducting airways characterized by TH2 inflammation and tissue remodeling after exposure to inhaled allergens. Although the TH2 profile is undisputed, the underlying molecular mechanisms leading to this abnormal TH2 profile remain largely unclear. MicroRNAs (miRNAs) are short noncoding RNAs that are important regulators of gene expression in the immune system. However, the role of miRNAs, specifically miR-155, in the regulation of allergic airway inflammation is unexplored.ObjectivesWe sought to assess the contribution of miR-155 in a mouse model of allergic airway inflammation.MethodsTo investigate a role for miR-155 in the regulation of allergic inflammation in vivo, we used miR-155 knockout (KO) and wild-type (WT) mice sensitized and exposed to ovalbumin.ResultsmiR-155 deficiency resulted in diminished eosinophilic inflammation and mucus hypersecretion in the lungs of allergen-sensitized and allergen-challenged mice compared with WT control animals. This was supported by a reduction in TH2 cell numbers and airway TH2 cytokine levels and complete abrogation of allergen-induced airway eotaxin-2/CCL24 and periostin levels in miR-155 KO mice. Intranasal instillation of eotaxin-2/CCL24 before allergen challenge partially restored airway eosinophilia in miR-155 KO mice, and adoptive transfer of CD4+ T cells resulted in a similar degree of airway eosinophilia in miR-155 KO and WT mice. Furthermore, the transcription factor PU.1, a negative regulator of TH2 cytokine production, was upregulated in the airways of allergen-challenged miR-155 KO mice compared with WT mice.ConclusionsOur data provides evidence that miR-155 contributes to the regulation of allergic airway inflammation by modulating TH2 responses through the transcription factor PU.1. Allergic asthma is a chronic disease of the conducting airways characterized by TH2 inflammation and tissue remodeling after exposure to inhaled allergens. Although the TH2 profile is undisputed, the underlying molecular mechanisms leading to this abnormal TH2 profile remain largely unclear. MicroRNAs (miRNAs) are short noncoding RNAs that are important regulators of gene expression in the immune system. However, the role of miRNAs, specifically miR-155, in the regulation of allergic airway inflammation is unexplored. We sought to assess the contribution of miR-155 in a mouse model of allergic airway inflammation. To investigate a role for miR-155 in the regulation of allergic inflammation in vivo, we used miR-155 knockout (KO) and wild-type (WT) mice sensitized and exposed to ovalbumin. miR-155 deficiency resulted in diminished eosinophilic inflammation and mucus hypersecretion in the lungs of allergen-sensitized and allergen-challenged mice compared with WT control animals. This was supported by a reduction in TH2 cell numbers and airway TH2 cytokine levels and complete abrogation of allergen-induced airway eotaxin-2/CCL24 and periostin levels in miR-155 KO mice. Intranasal instillation of eotaxin-2/CCL24 before allergen challenge partially restored airway eosinophilia in miR-155 KO mice, and adoptive transfer of CD4+ T cells resulted in a similar degree of airway eosinophilia in miR-155 KO and WT mice. Furthermore, the transcription factor PU.1, a negative regulator of TH2 cytokine production, was upregulated in the airways of allergen-challenged miR-155 KO mice compared with WT mice. Our data provides evidence that miR-155 contributes to the regulation of allergic airway inflammation by modulating TH2 responses through the transcription factor PU.1." @default.
• W2140709510 created "2016-06-24" @default.
• W2140709510 creator A5005478064 @default.
• W2140709510 creator A5005888467 @default.
• W2140709510 creator A5012264811 @default.
• W2140709510 creator A5043330317 @default.
• W2140709510 creator A5054626777 @default.
• W2140709510 creator A5063855542 @default.
• W2140709510 creator A5086921129 @default.
• W2140709510 date "2014-05-01" @default.
• W2140709510 modified "2023-10-17" @default.
• W2140709510 title "MicroRNA-155 is essential for TH2-mediated allergen-induced eosinophilic inflammation in the lung" @default.
• W2140709510 cites W1526700155 @default.
• W2140709510 cites W1555985183 @default.
• W2140709510 cites W180810881 @default.
• W2140709510 cites W1902390994 @default.
• W2140709510 cites W1928347998 @default.
• W2140709510 cites W1966054625 @default.
• W2140709510 cites W1966288602 @default.
• W2140709510 cites W1968444292 @default.
• W2140709510 cites W1970365072 @default.
• W2140709510 cites W1988140132 @default.
• W2140709510 cites W1989245810 @default.
• W2140709510 cites W1995552142 @default.
• W2140709510 cites W2006744847 @default.
• W2140709510 cites W2007031153 @default.
• W2140709510 cites W2007711648 @default.
• W2140709510 cites W2010777881 @default.
• W2140709510 cites W2014869583 @default.
• W2140709510 cites W2014946489 @default.
• W2140709510 cites W2018058053 @default.
• W2140709510 cites W2027285027 @default.
• W2140709510 cites W2027746633 @default.
• W2140709510 cites W2028994878 @default.
• W2140709510 cites W2035908500 @default.
• W2140709510 cites W2042470241 @default.
• W2140709510 cites W2045904496 @default.
• W2140709510 cites W2050155729 @default.
• W2140709510 cites W2056835764 @default.
• W2140709510 cites W2059691278 @default.
• W2140709510 cites W2059901199 @default.
• W2140709510 cites W2060702086 @default.
• W2140709510 cites W2060763719 @default.
• W2140709510 cites W2061808825 @default.
• W2140709510 cites W2063801679 @default.
• W2140709510 cites W2064300792 @default.
• W2140709510 cites W2080176520 @default.
• W2140709510 cites W2085441977 @default.
• W2140709510 cites W2088661593 @default.
• W2140709510 cites W2120586951 @default.
• W2140709510 cites W2121873857 @default.
• W2140709510 cites W2133571578 @default.
• W2140709510 cites W2135152690 @default.
• W2140709510 cites W2137881107 @default.
• W2140709510 cites W2150435395 @default.
• W2140709510 cites W2152257387 @default.
• W2140709510 doi "https://doi.org/10.1016/j.jaci.2013.11.008" @default.
• W2140709510 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/24373357" @default.
• W2140709510 hasPublicationYear "2014" @default.
• W2140709510 type Work @default.
• W2140709510 sameAs 2140709510 @default.
• W2140709510 citedByCount "176" @default.
• W2140709510 countsByYear W21407095102014 @default.
• W2140709510 countsByYear W21407095102015 @default.
• W2140709510 countsByYear W21407095102016 @default.
• W2140709510 countsByYear W21407095102017 @default.
• W2140709510 countsByYear W21407095102018 @default.
• W2140709510 countsByYear W21407095102019 @default.
• W2140709510 countsByYear W21407095102020 @default.
• W2140709510 countsByYear W21407095102021 @default.
• W2140709510 countsByYear W21407095102022 @default.
• W2140709510 countsByYear W21407095102023 @default.
• W2140709510 crossrefType "journal-article" @default.
• W2140709510 hasAuthorship W2140709510A5005478064 @default.
• W2140709510 hasAuthorship W2140709510A5005888467 @default.
• W2140709510 hasAuthorship W2140709510A5012264811 @default.
• W2140709510 hasAuthorship W2140709510A5043330317 @default.
• W2140709510 hasAuthorship W2140709510A5054626777 @default.
• W2140709510 hasAuthorship W2140709510A5063855542 @default.
• W2140709510 hasAuthorship W2140709510A5086921129 @default.
• W2140709510 hasConcept C189165786 @default.
• W2140709510 hasConcept C203014093 @default.
• W2140709510 hasConcept C207480886 @default.
• W2140709510 hasConcept C2776042228 @default.
• W2140709510 hasConcept C2776090121 @default.
• W2140709510 hasConcept C2776914184 @default.
• W2140709510 hasConcept C2776946954 @default.
• W2140709510 hasConcept C2777037409 @default.
• W2140709510 hasConcept C2777129736 @default.
• W2140709510 hasConcept C2777699602 @default.
• W2140709510 hasConcept C2777716647 @default.
• W2140709510 hasConcept C2778690821 @default.
• W2140709510 hasConcept C2779675166 @default.
• W2140709510 hasConcept C2779727006 @default.
• W2140709510 hasConcept C2780510475 @default.
• W2140709510 hasConcept C71924100 @default.
• W2140709510 hasConcept C86803240 @default.
• W2140709510 hasConcept C8891405 @default.

• next