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. 2008 May 12;205(5):1109–1120. doi: 10.1084/jem.20072000

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© 2008 Yamashita et al.

This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.jem.org/misc/terms.shtml). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).

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Figure 7. — Decreased mucus hyperproduction and airway hyperresponsiveness in Bmi1^−/− memory Th2 mice. Bmi1^+/+ and Bmi1^−/− memory Th2 mice were challenged by inhalation with OVA as in Fig. 5. (A) 1 d after the last OVA inhalation (day 11), the lungs were fixed and stained with periodic-acid-Schiff (PAS). A representative staining pattern is shown. The control represents BALB/c nu/nu mice without Th2 cell transfer. Bars, 100 μm. (B) On day 12, total RNA was prepared from the lung, and the expression of Gob5, Muc5a/c, and Muc 5b (molecular makers for Goblet cell hyperplasia and mucus production) was determined by a quantitative PCR analysis. The relative intensity (/HPRT; mean of three samples) is shown with standard deviations. (C) OVA-induced airway hyperresponsiveness in Bmi1^−/− memory Th2 mice. On day 11, the airway hyperresponsiveness in response to increasing doses of methacholine was measured in a whole-body plethysmograph. The mean values (n = 5) are shown with standard deviations. PBS, PBS-inhaled control; OVA, OVA-inhaled. *, P < 0.01. The experiments were performed twice with similar results. (D) On day 11, changes in the RL (left) and the dynamic compliance (Cdyn; right) were assessed. Mean values (six mice per group) are shown with standard deviations. *, P < 0.01; **, P < 0.05.