β-Arrestin-2 regulates the development of allergic asthma
J. Clin. Invest. Julia K.L. Walker, et al. 112:566 doi:10.1172/JCI17265 [Go to this article.]

Figure 2
Effect of OVA treatment on airway inflammation. (a) Effect of genotype and OVA treatment on lung inflammation evaluated by histological analysis of lung sections. Lung sections from WT-alum (lower left) and βarr2^–/–-alum mice (lower right) appeared normal with no inflammatory cell infiltration. Lung sections from WT-OVA mice (upper left) showed severe cellular infiltration in the interstitium. Lung sections from βarr2^–/–-OVA mice (upper right) showed mild extravasation of inflammatory cells in the interstitium. Representative histological sections are shown (n = 8–11 mice per group). (b) Representative images of cross-sectioned airways together with peribronchovascular connective tissue are shown. CD3⁺ T cells were counted in the subtended bronchovascular interstitium. OVA-treated WT mice showed an increased number of CD3⁺ T cells in the peribronchovascular zone relative to alum-treated mice. No such infiltration of CD3⁺ T cells was observed in OVA-treated βarr2^–/– mice. (c) Effect of genotype and OVA treatment on lung inflammation assessed by identification of cells harvested from whole-lung lavage. Black bars represent WT-OVA mice; white bars represent βarr2^–/–-OVA mice; light gray bars represent WT-alum mice; dark gray bars represent βarr2^–/–-alum mice. Data are mean ± SEM; n = 9–12 mice per group. *P < 0.05 versus all other groups.