Fig 7. Effect of B3B4 Ab targeting of airway CD23 on airway allergic inflammation.

WT mice were sensitized with OVA and received i.n. inoculation of 75 µg B3B4 Ab or rat IgG2a in PBS twice, once at 24 h before and again 1 h before challenge. Subsequently, mice were challenged with OVA and 24 h later AHR was measured, and 48 h later mice were sacrificed and lung tissues were fixed in formalin and embedded in paraffin.

A. Lung sections were stained with H&E and examined by light microscopy at the indicated magnifications. Lung sections in B3B4 Ab-treated mice showed significant attenuation of inflammation in comparison with that of control rat IgG2a-treated mice. Insets (green squares) are shown at higher amplifications. Semi-quantitative assessment of inflammation in histological sections was analyzed (A2 panel). *P<0.05.

B. Lung tissue sections were stained using the Masson's trichrome method. B3B4 Ab-treated mice showed significantly decreased peribronchial fibrosis (blue) in the lung compared with control Ab-treated mice.

C. Lung tissue sections were stained with PAS. B3B4-treated mice had a significant reduction in goblet-cell hyperplasia in the lung bronchial area compared with that of the rat IgG2a-treated mice (c1). Goblet cells were counted and the mean percentage of three different sections is presented (c2). *P<0.01.

D. Airway responsiveness to methacholine (MCh) in B3B4 Ab-treated mice. AHR was measured 24 h after a single OVA challenge. First, baseline airway resistance and resistance against PBS challenge were measured and then a dose response curve against increasing concentrations of nebulized MCh (3–100 mg/ml) was generated. *P<0.05.