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- W2938688436 abstract "Asthma is a heterogeneous chronic inflammatorydisease characterised by recurrent, reversible airflowobstruction, bronchial hyperresponsiveness (BHR) and airway remodelling.Impaired lung function in childhood asthma has been associated withpolymorphisms in ADAM33 . Soluble ADAM33 (sADAM33) is increased inbronchial lavage fluid (BALF) from asthmatics and is inversely correlated with FEV1.sADAM33 is induced by TGF-β present in asthmatic lungs, andpromotes angiogenesis. ADAM33 expression is developmentally regulated and is influencedby maternal allergy via IL-13. This thesis will examine the hypothesis thatalteration in the expression of ADAM33 will influencelung structure, affecting vessel and smooth muscle formation and these subsequentchanges will impact on pulmonary function in airway inflammation. In DOX inducible Il-13 transgenic mice, significantneutrophilic inflammation and goblet cell metaplasia were observed. BHR was inducedafter methacholine challenge and IHC showed increased bronchial smooth muscle.Similarly, in human embryonic and juvenile mouse lungs, IL-13 suppressed Adam33 mRNA but not Acta2 . ADAM33 was identifiedin BALF of the overexpressing mice. ADAM33 enzymatic activity was also significantlyincreased. In the ADAM33 transgenic model, induction of ADAM33 resultedin enzymatically active sADAM33 in BALF. ADAM33 significantlyincreased the expression of fibrotic markerssuggesting regulation of pulmonary myogenesis, fibrogenesis,and angiogenesis. Consistent with this, immunofluorescencerevealed airway remodelling with increased smooth muscle, collagen depositionand vessel formation in ADAM33 mice. In contrast, inflammatorycell counts in BALF, expression of inflammatorymediators and mucus related genes were not altered by ADAM33 . In Adam33-/- challenged with HDM, there was less BHR and eosinophilic and neutrophilicinflammation compared to Adam33 +/+. HDM caused suppression of Adam33 mRNA as well as ectodomain shedding of ADAM33 protein in BALF of wildtype micethat was absent in Adam33 -/-. The study provides novel data showing expression of sADAM33 in airways toinduce myogenesis, fibrogenesis and angiogenesis, consistent with a process causingairway remodelling in the absence of inflammation." @default.
- W2938688436 created "2019-04-25" @default.
- W2938688436 creator A5061124905 @default.
- W2938688436 date "2014-03-01" @default.
- W2938688436 modified "2023-09-27" @default.
- W2938688436 title "Elucidating the role of ADAM33 in airway inflammation and remodelling in asthma" @default.
- W2938688436 hasPublicationYear "2014" @default.
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