• Michael Roth and Michael Tamm.
• Division of Pulmonary Cell Research, Department of Research, University Hospital Basel, Basel, Switzerland. rothmic@uhbs.ch
• Ann. Allergy Asthma Immunol. 2010 Feb 1; 104 (2): 152-60.

BackgroundHuman airway smooth muscle cells (ASMCs) express high- and low-affinity IgE receptors and respond to IgE, thereby contributing to airway inflammation.ObjectiveTo determine whether anti-IgE antibodies (omalizumab) block the response of ASMCs to IgE in patients with asthma.MethodsAirway smooth muscle cells, isolated from the biopsy specimens of patients with asthma, patients with chronic obstructive pulmonary disease, and control participants (6 in each group), were stimulated with IgE with and without omalizumab treatment, and cytokine secretion was determined by enzyme-linked immunosorbent assay, and messenger RNA (mRNA) secretion by real-time polymerase chain reaction, over 24 hours. IgE receptor expression was determined by immunoblotting.ResultsIgE-stimulated mRNA synthesis encoded for interleukin (IL) 6, IL-8, and tumor necrosis factor a in ASMCs via mitogen-activated protein kinases, extracellular signal-regulated kinase 1/2, or p38. The secretion of the respective cytokines increased significantly: IL-6, IL-8, and tumor necrosis factor a at 6 hours and IL-4 at 24 hours. Cytokine mRNA synthesis and protein secretion were inhibited by omalizumab in a dose-dependent manner. The expression of low- and high-affinity IgE receptors was not altered by omalizumab in ASMCs.ConclusionsOmalizumab reduced IgE-stimulated synthesis and secretion of proinflammatory cytokines by human ASMCs. These findings imply a beneficial action of omalizumab in asthma therapy. This effect is not restricted to inflammatory cells; it also includes tissue-forming cells.

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