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Activation of human lung mast cells by monomeric immunoglobulin E

Institute for Lung Health, Dept of Infection, Immunity and Inflammation, University of Leicester and Warwick Medical School, University Hospitals of Leicester, Glenfield General Hospital, Leicester, UK

CORRESPONDENCE: P. Bradding, Dept of Respiratory Medicine, Glenfield Hospital, Groby Rd, Leicester, LE3 9QP, UK. Fax: 44 1162502787. E-mail: pbradding@hotmail.com

Keywords: Asthma, calcium, human, mast cell, mediators, monomeric immunoglobulin E

Received: August 3, 2004
Accepted January 20, 2005

The mechanism of chronic mast cell activation in asthma is unclear. Monomeric immunoglobulin (Ig)E in the absence of allergen induces mediator release from rodent mast cells, indicating a possible role for IgE in the continued activation of mast cells within the asthmatic bronchial mucosa. In this study it was investigated whether monomeric IgE induces Ca²⁺ influx and mediator release from human lung mast cells (HLMC).

Purified HLMC were cultured for 4 weeks and then exposed to monomeric human myeloma IgE. Ratiometric Ca²⁺ imaging was performed on single fura-2-loaded cells. Histamine release was measured by radioenzymatic assay; leukotriene C₄ (LTC₄) and interleukin (IL)-8 were measured by ELISA.

At concentrations experienced in vivo, monomeric IgE induced dose-dependent histamine release, LTC₄ production and IL-8 synthesis. This was associated with a rise in cytosolic free Ca²⁺. Enhanced histamine release was still evident 1 week after initial exposure to IgE suggesting that continued exposure maintains enhanced secretion.

Monomeric immunoglobulin E alone activates cultured human lung mast cells initiating Ca²⁺ influx, degranulation, arachidonic acid metabolism and cytokine synthesis. These findings support the hypothesis that immunoglobulin E loading of mast cells within the asthmatic airway contributes to the disordered airway physiology of this disease.

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