Anaphylactic Reactions to Oligosaccharides in Red Meat: a Syndrome in Evolution

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.