Pretreatment with (R)-albuterol before TNF-α significantly inhibits TNF-α-induced ICAM-1 mRNA expression in human parasympathetic neurons as detected by real-time qPCR (A).

<p>(S)-or (R,S)-albuterol does not inhibit TNF-α induced ICAM-1 (A). The inhibitory effect of (R)-albuterol on TNF-α-induced ICAM-1 mRNA expression is dose dependent (B). Neither TNF-α nor any albuterol isomer changes eotaxin expression (C). *indicates significantly different from control. **indicates significantly different from TNF-α treatment, as analyzed by one way ANOVA.</p

β₂ receptors are identified by anti-β₂ receptors antibody on human trachea parasympathetic neurons (red, A, B–D) under high (A,C) and low (D) power.

<p>Neurons are labeled with anti-neurofilament antibodis (B, green) and the merged image (for neuronal and β₂ receptor staining) is shown in C. Nuclei stain blue with DAPI. The insert of D is the absence of primary antibody. Magnification bars: 50 µm.</p

ICAM-1 protein expression is measured by fluorescence intensity of a labeled anti-ICAM-1 antibody.

<p>(R)-albuterol (A) but not S- or (R-,S)-albuterol (B and C) significantly inhibits TNF-α-induced ICAM-1 protein (p<0.005). *indicates significantly different from control and **indicates significantly different from TNF- treatment, as analyzed by paired T-test.</p

Pretreatment with β-receptor antagonist propranolol completely prevents the suppressive effect of R-albuterol on TNF-α-induced ICAM-1 protein expression that is identified by fluorescence intensity of anti-ICAM-1 antibody staining in human parasympathetic nerves.

<p>*indicates significant difference from control, ** indicates significant difference from TNF-α treatment and *** indicates significant difference from (R)-albuterol, as analyzed by one way ANOVA.</p