Histamine Promotes the Release of Interleukin-6 via the H1R/p38 and NF-kappa B Pathways in Nasal Fibroblasts
- Authors
- Park, Ii-Ho; Um, Ji-Young; Cho, Jung-Sun; Lee, Seung Hoon; Lee, Sang Hag; Lee, Heung-Man
- Issue Date
- 11월-2014
- Publisher
- KOREAN ACAD ASTHMA ALLERGY & CLINICAL IMMUNOLOGY
- Keywords
- Nose; fibroblast; histamine; IL-6; allergic rhinitis
- Citation
- ALLERGY ASTHMA & IMMUNOLOGY RESEARCH, v.6, no.6, pp.567 - 572
- Indexed
- SCIE
SCOPUS
KCI
- Journal Title
- ALLERGY ASTHMA & IMMUNOLOGY RESEARCH
- Volume
- 6
- Number
- 6
- Start Page
- 567
- End Page
- 572
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/96942
- DOI
- 10.4168/aair.2014.6.6.567
- ISSN
- 2092-7355
- Abstract
- Purpose: Based on the close relationship between histamine and interleukin 6 (IL-6), we hypothesized that histamine may regulate the production of cytokines, such as IL-6, during allergic inflammation. Here, we examined the role of histamine in IL-6 production and histamine receptor activity in nasal fibroblasts, along with the mechanisms underlying these effects. Methods: Experiments were performed using nasal fibroblasts from 8 normal patients. RT-PCR was used to identify the major histamine receptors expressed in nasal fibroblasts. Fibroblasts were then treated with histamine with or without histamine-receptor antagonists, and monitored for IL-6 production using an ELISA. Four potential downstream signaling molecules, p38, extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and NF-kappa B, were evaluated by Western blot, and a luciferase reporter assay. Results: Elevated expression was seen for all histamine receptors, with IL-6 protein levels increasing significantly following histamine stimulation. Among the histamine-receptor specific antagonists, only the H1R antagonist significantly decreased IL-6 production in histaminestimulated nasal fibroblasts. Histamine increased the expression level of phosphorylated p38 (pp38), pERK, and pJNK, as well as NF-K kappa B induction. The H1R antagonist actively suppressed pp38 and NF-kappa B expression in histamine-induced nasal fibroblasts, but not pERK and pJNK. The p38 inhibitor strongly attenuated IL-6 production in histamine-stimulated nasal fibroblasts. Conclusions: The data presented here suggest that antihistamines may be involved in the regulation of cytokines, such as IL-6, due to the role of histamine as an inflammatory mediator in nasal fibroblasts.
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Collections - College of Medicine > Department of Medical Science > 1. Journal Articles
- Graduate School > Department of Biomedical Sciences > 1. Journal Articles
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