House Dust Mite Induces Expression of Intercellular Adhesion Molecule-1 in EoL-1 Human Eosinophilic Leukemic Cells

The house dust mite (HDM) is considered to be the most common indoor allergen associated with bronchial asthma. In this study, we investigated whether crude extract of the HDM Dermatophagoides farinae could activate human eosinophilic leukemic cells (EoL-1) to induce upregulation of cell-surface adhesion molecules. When EoL-1 cells were incubated with D. farinae extract, expression of intercellular adhesion molecule-1 (ICAM-1) significantly increased on the cell surfaces compared to cells incubated with medium alone. In contrast, surface expression of CD11b and CD49d in EoL-1 cells was not affected by D. farinae extract. In addition, pretreatment of cells with NF-κB inhibitor (MG-132) or JNK inhibitor (SP600125) significantly inhibited ICAM-1 expression promoted by HDM extract. However, neither p38 MAP kinase inhibitor nor MEK inhibitor prevented HDM-induced ICAM-1 expression in EoL-1 cells. These results suggest that crude extract of D. farinae induces ICAM-1 expression in EoL-1 cells through signaling pathways involving both NF-κB and JNK

Contracted Nose after Silicone Implantation: A New Classification System and Treatment Algorithm

Background Silicone implants are frequently used in augmentation rhinoplasty in Asians. A common complication of silicone augmentation rhinoplasty is capsular contracture. This is similar to the capsular contracture after augmentation mammoplasty, but a classification for secondary contracture after augmentation rhinoplasty with silicone implants has not yet been established, and treatment algorithms by grade or severity have yet to be developed. Methods Photographs of 695 patients who underwent augmentation rhinoplasty with a silicone implant from May 2001 to May 2015 were analyzed. The mean observation period was 11.4 months. Of the patients, 81 were male and 614 were female, with a mean age of 35.9 years. Grades were assigned according to postoperative appearance. Grade I was a natural appearance, as if an implant had not been inserted. Grade II was an unnatural lateral margin of the implant. Clearly identifiable implant deviation was classified as grade III, and short nose deformation was grade IV. Results Grade I outcomes were found in 498 patients (71.7%), grade II outcomes in 101 (14.5%), grade III outcomes in 75 (10.8%), and grade IV outcomes in 21 patients (3.0%). Revision surgery was indicated for the 13.8% of all patients who had grade III or IV outcomes. Conclusions It is important to clinically classify the deformations due to secondary contracture after surgery and to establish treatment algorithms to improve scientific communication among rhinoplasty surgeons. In this study, we suggest guidelines for the clinical classification of secondary capsular contracture after augmentation rhinoplasty, and also propose a treatment algorithm

The Effects of Melittin and Apamin on Airborne Fungi-Induced Chemical Mediator and Extracellular Matrix Production from Nasal Polyp Fibroblasts

Melittin and apamin are the main components of bee venom and they have been known to have anti-inflammatory and anti-fibrotic properties. The aim of this study was to evaluate the effect of melittin and apamin on airborne fungi-induced chemical mediator and extracellular matrix (ECM) production in nasal fibroblasts. Primary nasal fibroblasts were isolated from nasal polyps, which were collected during endoscopic sinus surgery. Nasal fibroblasts were treated with Alternaria and Aspergillus. The effects of melittin and apamin on the production of interleukin (IL)-6 and IL-8 were determined with enzyme linked immunosorbent assay. ECM mRNA and protein expressions were determined with the use of quantitative RT-PCR and Western blot. Alternaria-induced IL-6 and IL-8 production was significantly inhibited by apamin. However, melittin did not influence the production of IL-6 and IL-8 from nasal fibroblasts. Melittin or apamin significantly inhibited collagen type I, TIMP-1, and MMP-9 mRNA expression and protein production from nasal fibroblasts. Melittin and apamin inhibited Alternaria-induced phosphorylation of Smad 2/3 and p38 MAPK. Melittin and apamin can inhibit the fungi-induced production of chemical mediators and ECM from nasal fibroblasts. These results suggest the possible role of melittin and apamin in the treatment of fungi induced airway inflammatory diseases