Abstract
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.
Highlights
Nasal polyps are swellings and there is damage to the mucosal epithelium with inflammatory cell infiltration
Alternaria and Aspergillus are known common pathogens found in nasal secretion and they induce the production of chemical mediators from nasal epithelial
Melittin and apamin are the well-known components of be important venom (BV)
Summary
Nasal polyps are swellings and there is damage to the mucosal epithelium with inflammatory cell infiltration. The pathogenesis of nasal polyps is not fully understood, mucosal epithelial damage, extracellular matrix (ECM) accumulation, and increased local inflammatory mediators are the characteristic pathophysiologic findings of nasal polyps [1]. Fibroblasts are the main structural components of the nasal mucosa and they participate in the local immune response through the production of biological mediators which are involved in the recruitment of inflammatory cells and the cellular source of ECM proteins [2]. Fungi are commonly found in the nasal mucosa and relatively few species are implicated in airway inflammatory disease. Alternaria and Aspergillus are known common pathogens found in nasal secretion and they induce the production of chemical mediators from nasal epithelial
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