Abstract
Background: Cigarette smoke exposure has been reported to influence allergic immune responses. Confusingly, both attenuation and exacerbation of allergic responses have been shown. Since mast cells are central regulators of allergic reactions and innate immunity, we have studied the effects of cigarette smoke medium (CSM) on mast cells after allergic activation. Material and Methods: Primary cultured murine mast cells were exposed to CSM and activated with IgE and antigen or lipopolysaccharide (LPS). The releases of granules, production of leukotrienes, chemokines and cytokines was determined in supernatants by ELISA. The effect of CSM exposure on intracellular signaling, especially the NF-κB and Erk1/2 pathways, was analyzed by Western blotting. Results: CSM suppressed IgE-mediated degranulation and cytokine release, but no effect was observed on leukotriene release. CSM induced phosphorylation of Erk1/2 in mast cells. In CSM-exposed mast cells ATF-1 was phosphorylated after stimulation with IgE/Ag. LPS activated mast cells were not influenced by CSM. Conclusion: Our study suggests that exposure to cigarette smoke may lead to a reduced allergic activation of mast cells without affecting their response to activation via e.g. bacterial derived LPS.
Original language | English |
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Pages | 138 |
Number of pages | 1 |
DOIs | |
Publication status | Published - 1 Jun 2009 |
Keywords
- cigarette smoke
- lipopolysaccharide
- leukotriene
- immunoglobulin E
- antigen
- cytokine
- chemokine
- mast cell
- allergy
- clinical immunology
- exposure
- allergic reaction
- phosphorylation
- degranulation
- Western blotting
- intracellular signaling
- innate immunity
- attenuation
- cytokine release
- immune response
- stimulation
- enzyme linked immunosorbent assay