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Enhanced effects of cigarette smoke extract on inflammatory cytokine... » Isaúde
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Name of the journal:   Volume:   Number:
Clinical and Molecular Allergy
0000-00-00 00:00:00

Enhanced effects of cigarette smoke extract on inflammatory cytokine expression in IL-1beta-activated human mast cells were inhibited by Baicalein via regulation of the NF-kappaB pathway

Description: Background:Human mast cells are capable of a wide variety of inflammatory responses and play a vital role in the pathogenesis of inflammatory diseases such as allergy, asthma, and atherosclerosis. We have reported that cigarette smoke extract (CSE) significantly increased IL-6 and IL-8 production in IL-1--activated human mast cell line (HMC-1). Baicalein (BAI) has anti-inflammatory properties and inhibits IL-1-- and TNF---induced inflammatory cytokine production from HMC-1. The goal of the present study was to examine the effect of BAI on IL-6 and IL-8 production from CSE-treated and IL-1--activated HMC-1.Methods:Main-stream (Ms) and Side-stream (Ss) cigarette smoke were collected onto fiber filters and extracted in RPMI-1640 medium. Two ml of HMC-1 at 1 ? 106 cells/mL were cultured with CSE in the presence or absence of IL-1- (10 ng/mL) for 24 hrs. A group of HMC-1 cells stimulated with both IL-1- (10 ng/ml) and CSE was also treated with BAI. The expression of IL-6 and IL-8 was assessed by ELISA and RT-PCR. NF--B activation was measured by electrophoretic mobility shift assay (EMSA) and I-B- degradation by Western blot.Results:Both Ms and Ss CSE significantly increased IL-6 and IL-8 production (p < 0.001) in IL-1--activated HMC-1. CSE increased NF--B activation and decreased cytoplasmic I-B- proteins in IL-1--activated HMC-1. BAI (1.8 to 30 -M) significantly inhibited production of IL-6 and IL-8 in a dose-dependent manner in IL-1--activated HMC-1 with the optimal inhibition concentration at 30 -M, which also significantly inhibited the enhancing effect of CSE on IL-6 and IL-8 production in IL-1--activated HMC-1. BAI inhibited NF--B activation and increased cytoplasmic I-B- proteins in CSE-treated and IL-1--activated HMC-1.Conclusions:Our results showed that CSE significantly increased inflammatory cytokines IL-6 and IL-8 production in IL-1--activated HMC-1. It may partially explain why cigarette smoke contributes to lung and cardiovascular diseases. BAI inhibited the production of inflammatory cytokines through inhibition of NF--B activation and I-B- phosphorylation and degradation. This inhibitory effect of BAI on the expression of inflammatory cytokines induced by CSE suggests its usefulness in the development of novel anti-inflammatory therapies.

Identifier: doi:10.1186/1476-7961-10-3
Volume: 0
Page: 3 a


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