Mechanisms of allergy and clinical immunologyInduction of a disintegrin and metalloprotease 33 during embryonic lung development and the influence of IL-13 or maternal allergy
Section snippets
Methods
Additional details of all Methods can be found in this article's Online Repository at www.jacionline.org.
ADAM33 mRNA expression in HELs in vivo
To study the expression of ADAM33 mRNA in HELs, RNA was extracted from fresh HELs obtained 7 to 9 weeks postconception. Comparisons during the early pseudoglandular stage of lung development suggested that ADAM33 mRNA expression increased significantly from 7 to 9 weeks postconception (Fig 1, A). When HEL tissues were dissected into the tubular structure and the mesenchyme surrounding these structures, ADAM33 mRNA expression was significantly higher in the mesenchyme (Fig 1, B), confirming our
Discussion
In this study, we show for the first time that ADAM33/Adam33 expression is developmentally regulated in human and murine lungs. Furthermore, although mRNA expression is suppressed by maternal allergy or exogenous IL-13, in vivo Adam33 protein is increased in lungs from 4-day-old offspring of mothers with ovalbumin allergy, suggesting important gene-environment interactions that may contribute to asthma pathogenesis. We have previously shown that ADAM33 can be found almost exclusively in the
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2020, Journal of Allergy and Clinical ImmunologyCitation Excerpt :Postnatally, Sftpa expression was not determined, as analysis of Sftpc expression provides sufficient insight into the maturation of AEC type II, which showed no significant differences between groups. Next, the expression of the transcription factor SRY-Box 9 (Sox9), which is involved in the transition from branching morphogenesis to alveolar epithelial terminal differentiation,63 and disintegrin and metalloproteinase domain-containing protein 33 (Adam33), an asthma susceptibility gene associated with lung development,64 was assessed. Prenatal stress challenge did not significantly affect the expression of these markers, but a reduced expression pattern was observed in the female lung (see Fig E6, F).
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Disclosure of potential conflict of interest: D. J. P. Bassett and X. Gao have received research support from the Michigan University Challenge Initiative, Synairgen Research Ltd, and Wayne State University Research Enhancement. D. I. Wilson has received research support from the Engineering and Physical Sciences Research Council UK. The rest of the authors have declared that they have no conflict of interest.
Supported by the Asthma, Allergy and Inflammation Research (AAIR) Charity, the British Lung Foundation, the Medical Research Council, and the Roger Brooke Charitable Trust, United Kingdom; and Research Enhancement Funds, Wayne State University, Detroit, Mich.