FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W1409144667> ?p ?o ?g. }

• W1409144667 endingPage "578" @default.
• W1409144667 startingPage "571" @default.
• W1409144667 abstract "BackgroundAsthmatic patients are highly susceptible to air pollution and in particular to the effects of ozone (O3) inhalation, but the underlying mechanisms remain unclear.ObjectiveUsing mouse models of O3-induced airway inflammation and airway hyperresponsiveness (AHR), we sought to investigate the role of the recently discovered group 2 innate lymphoid cells (ILC2s).MethodsC57BL/6 and BALB/c mice were exposed to Aspergillus fumigatus, O3, or both (3 ppm for 2 hours). ILC2s were isolated by means of fluorescence-activated cell sorting and studied for Il5 and Il13 mRNA expression. ILC2s were depleted with anti-Thy1.2 mAb and replaced by means of intratracheal transfer of ex vivo expanded Thy1.1 ILC2s. Cytokine levels (ELISA and quantitative PCR), inflammatory cell profile, and AHR (flexiVent) were assessed in the mice.ResultsIn addition to neutrophil influx, O3 inhalation elicited the appearance of eosinophils and IL-5 in the airways of BALB/c but not C57BL/6 mice. Although O3-induced expression of IL-33, a known activator of ILC2s, in the lung was similar between these strains, isolated pulmonary ILC2s from O3-exposed BALB/c mice had significantly greater Il5 and Il13 mRNA expression than C57BL/6 mice. This suggested that an altered ILC2 function in BALB/c mice might mediate the increased O3 responsiveness. Indeed, anti-Thy1.2 treatment abolished but ILC2s added back dramatically enhanced O3-induced AHR.ConclusionsO3-induced activation of pulmonary ILC2s was necessary and sufficient to mediate asthma-like changes in BALB/c mice. This previously unrecognized role of ILC2s might help explain the heightened susceptibility of human asthmatic airways to O3 exposure. Asthmatic patients are highly susceptible to air pollution and in particular to the effects of ozone (O3) inhalation, but the underlying mechanisms remain unclear. Using mouse models of O3-induced airway inflammation and airway hyperresponsiveness (AHR), we sought to investigate the role of the recently discovered group 2 innate lymphoid cells (ILC2s). C57BL/6 and BALB/c mice were exposed to Aspergillus fumigatus, O3, or both (3 ppm for 2 hours). ILC2s were isolated by means of fluorescence-activated cell sorting and studied for Il5 and Il13 mRNA expression. ILC2s were depleted with anti-Thy1.2 mAb and replaced by means of intratracheal transfer of ex vivo expanded Thy1.1 ILC2s. Cytokine levels (ELISA and quantitative PCR), inflammatory cell profile, and AHR (flexiVent) were assessed in the mice. In addition to neutrophil influx, O3 inhalation elicited the appearance of eosinophils and IL-5 in the airways of BALB/c but not C57BL/6 mice. Although O3-induced expression of IL-33, a known activator of ILC2s, in the lung was similar between these strains, isolated pulmonary ILC2s from O3-exposed BALB/c mice had significantly greater Il5 and Il13 mRNA expression than C57BL/6 mice. This suggested that an altered ILC2 function in BALB/c mice might mediate the increased O3 responsiveness. Indeed, anti-Thy1.2 treatment abolished but ILC2s added back dramatically enhanced O3-induced AHR. O3-induced activation of pulmonary ILC2s was necessary and sufficient to mediate asthma-like changes in BALB/c mice. This previously unrecognized role of ILC2s might help explain the heightened susceptibility of human asthmatic airways to O3 exposure." @default.
• W1409144667 created "2016-06-24" @default.
• W1409144667 creator A5011069259 @default.
• W1409144667 creator A5019375210 @default.
• W1409144667 creator A5025705056 @default.
• W1409144667 creator A5026548451 @default.
• W1409144667 creator A5042456497 @default.
• W1409144667 creator A5043321798 @default.
• W1409144667 creator A5049637659 @default.
• W1409144667 creator A5055814385 @default.
• W1409144667 date "2016-02-01" @default.
• W1409144667 modified "2023-10-16" @default.
• W1409144667 title "Group 2 innate lymphoid cells mediate ozone-induced airway inflammation and hyperresponsiveness in mice" @default.
• W1409144667 cites W10370208 @default.
• W1409144667 cites W1928224582 @default.
• W1409144667 cites W1981862096 @default.
• W1409144667 cites W1998846885 @default.
• W1409144667 cites W2007790364 @default.
• W1409144667 cites W2009037588 @default.
• W1409144667 cites W2027462139 @default.
• W1409144667 cites W2032765714 @default.
• W1409144667 cites W2047263108 @default.
• W1409144667 cites W2048298616 @default.
• W1409144667 cites W2050321310 @default.
• W1409144667 cites W2053661306 @default.
• W1409144667 cites W2054052467 @default.
• W1409144667 cites W2059449238 @default.
• W1409144667 cites W2062783549 @default.
• W1409144667 cites W2067500883 @default.
• W1409144667 cites W2068022492 @default.
• W1409144667 cites W2076279510 @default.
• W1409144667 cites W2078498449 @default.
• W1409144667 cites W2079280811 @default.
• W1409144667 cites W2083215156 @default.
• W1409144667 cites W2087055101 @default.
• W1409144667 cites W2100908574 @default.
• W1409144667 cites W2101035994 @default.
• W1409144667 cites W2102191332 @default.
• W1409144667 cites W2106790228 @default.
• W1409144667 cites W2107023210 @default.
• W1409144667 cites W2109945923 @default.
• W1409144667 cites W2140206763 @default.
• W1409144667 cites W2140942460 @default.
• W1409144667 cites W2145818079 @default.
• W1409144667 cites W2147227296 @default.
• W1409144667 cites W2150464681 @default.
• W1409144667 cites W2152222824 @default.
• W1409144667 cites W2416664906 @default.
• W1409144667 cites W4319308391 @default.
• W1409144667 doi "https://doi.org/10.1016/j.jaci.2015.06.037" @default.
• W1409144667 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4747855" @default.
• W1409144667 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/26282284" @default.
• W1409144667 hasPublicationYear "2016" @default.
• W1409144667 type Work @default.
• W1409144667 sameAs 1409144667 @default.
• W1409144667 citedByCount "81" @default.
• W1409144667 countsByYear W14091446672016 @default.
• W1409144667 countsByYear W14091446672017 @default.
• W1409144667 countsByYear W14091446672018 @default.
• W1409144667 countsByYear W14091446672019 @default.
• W1409144667 countsByYear W14091446672020 @default.
• W1409144667 countsByYear W14091446672021 @default.
• W1409144667 countsByYear W14091446672022 @default.
• W1409144667 countsByYear W14091446672023 @default.
• W1409144667 crossrefType "journal-article" @default.
• W1409144667 hasAuthorship W1409144667A5011069259 @default.
• W1409144667 hasAuthorship W1409144667A5019375210 @default.
• W1409144667 hasAuthorship W1409144667A5025705056 @default.
• W1409144667 hasAuthorship W1409144667A5026548451 @default.
• W1409144667 hasAuthorship W1409144667A5042456497 @default.
• W1409144667 hasAuthorship W1409144667A5043321798 @default.
• W1409144667 hasAuthorship W1409144667A5049637659 @default.
• W1409144667 hasAuthorship W1409144667A5055814385 @default.
• W1409144667 hasBestOaLocation W14091446671 @default.
• W1409144667 hasConcept C105702510 @default.
• W1409144667 hasConcept C122862929 @default.
• W1409144667 hasConcept C126322002 @default.
• W1409144667 hasConcept C136449434 @default.
• W1409144667 hasConcept C185592680 @default.
• W1409144667 hasConcept C203014093 @default.
• W1409144667 hasConcept C2776178081 @default.
• W1409144667 hasConcept C2776238763 @default.
• W1409144667 hasConcept C2776914184 @default.
• W1409144667 hasConcept C2776954882 @default.
• W1409144667 hasConcept C2777714996 @default.
• W1409144667 hasConcept C2778070265 @default.
• W1409144667 hasConcept C2778690821 @default.
• W1409144667 hasConcept C47742525 @default.
• W1409144667 hasConcept C71924100 @default.
• W1409144667 hasConcept C74172505 @default.
• W1409144667 hasConcept C86803240 @default.
• W1409144667 hasConcept C8891405 @default.
• W1409144667 hasConceptScore W1409144667C105702510 @default.
• W1409144667 hasConceptScore W1409144667C122862929 @default.
• W1409144667 hasConceptScore W1409144667C126322002 @default.
• W1409144667 hasConceptScore W1409144667C136449434 @default.
• W1409144667 hasConceptScore W1409144667C185592680 @default.
• W1409144667 hasConceptScore W1409144667C203014093 @default.

• next