BackgroundHuman 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-1β-activated human mast cell line (HMC-1). Baicalein (BAI) has anti-inflammatory properties and inhibits IL-1β- and TNF-α-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-1β-activated HMC-1.MethodsMain-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-1β (10 ng/mL) for 24 hrs. A group of HMC-1 cells stimulated with both IL-1β (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-κB activation was measured by electrophoretic mobility shift assay (EMSA) and IκBα degradation by Western blot.ResultsBoth Ms and Ss CSE significantly increased IL-6 and IL-8 production (p < 0.001) in IL-1β-activated HMC-1. CSE increased NF-κB activation and decreased cytoplasmic IκBα proteins in IL-1β-activated HMC-1. BAI (1.8 to 30 μM) significantly inhibited production of IL-6 and IL-8 in a dose-dependent manner in IL-1β-activated HMC-1 with the optimal inhibition concentration at 30 μM, which also significantly inhibited the enhancing effect of CSE on IL-6 and IL-8 production in IL-1β-activated HMC-1. BAI inhibited NF-κB activation and increased cytoplasmic IκBα proteins in CSE-treated and IL-1β-activated HMC-1.ConclusionsOur results showed that CSE significantly increased inflammatory cytokines IL-6 and IL-8 production in IL-1β-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-κB activation and IκBα 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.

Layer‐by‐layer (LBL) assembly of functionalized nanoparticles (FNPs) within a polyelectrolyte network is described (see image). The LBL‐NP‐assembly‐based modification can be used to engineer surfaces with multiple functions such as controlled (multiple‐) drug release with distinct release kinetics and enhanced contrast in clinical imaging modalities. This novel surface modification strategy is expected to accelerate the development of bioresponsive coatings for implantable biomedical devices.

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Peutz-Jeghers syndrome is a rare autosomal dominant syndrome associated with mucocutaneous pigmentation and hamartomatous gastrointestinal polyps. The syndrome is associated with increased risk for intestinal and extraintestinal malignancy. Peutz-Jeghers polyps have been found involving the stomach, small intestine, and colon. These polyps have a distinct arborizing pattern composed of smooth muscle derived from the muscularis mucosae with overlying nondysplastic epithelium. A subset of Peutz-Jeghers polyps demonstrate pseudoinvasion, which can lead to an improper diagnosis of malignancy. Properly identifying this mimicker of adenocarcinoma is essential for appropriate patient care. The variable clinical manifestations and diffuse location of Peutz-Jeghers polyps make proper identification and management challenging. This review addresses the history, pathology, clinical features, genetic abnormalities, and recommendations for surveillance and management.