IL-13 suppresses MUC5AC gene expression and mucin secretion in nasal epithelial cells

Chang-Hoon Kim, K. Seob Song, J. S. Koo, H. U. Kim, J. Y. Choi, H. J. Kim, J. H. Yoon

Research output: Contribution to journalArticle

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Abstract

Recently, it was found that IL-13 is involved in allergic inflammation and mucus hypersecretion in in vivo animal models. However, the role of IL-13 in in vitro cellular models has yet to be determined. This study aimed to investigate the direct effect of IL-13 on mucin gene expression and mucin secretion in cultured normal human nasal epithelial cells. After treatment with IL-13, total mucin and MUC5AC mucin levels were measured using an immunoblotting assay. MUC2, MUC5AC and MUC8 mRNA expression were determined using reverse transcription-polymerase chain reaction. Also, immunostaining was performed using a MUC5AC antibody on histologic and cytospin slides. After treatment with ≥ 5 ng/ml IL-13, the level of total mucin and MUC5AC mucin secretion decreased substantially. The expression of MUC2 and MUC8 mRNA increased with higher concentrations of IL-13, but the expression of MUC5AC mRNA decreased. On the 7th day after IL-13 treatment, a significant decrease in the number of MUC5AC-positive cells was confirmed by immunostaining. These findings indicate that IL-13 suppresses MUC5AC mucin gene expression and mucin secretion in cultured normal human nasal epithelial cells in vitro.

Original languageEnglish
Pages (from-to)638-643
Number of pages6
JournalActa Oto-Laryngologica
Volume122
Issue number6
DOIs
Publication statusPublished - 2002 Oct 29

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Interleukin-13
Mucins
Nose
Epithelial Cells
Gene Expression
Messenger RNA
Mucus
Immunoblotting
Reverse Transcription
Animal Models
Inflammation
Polymerase Chain Reaction
Antibodies

All Science Journal Classification (ASJC) codes

  • Otorhinolaryngology

Cite this

Kim, C-H., Seob Song, K., Koo, J. S., Kim, H. U., Choi, J. Y., Kim, H. J., & Yoon, J. H. (2002). IL-13 suppresses MUC5AC gene expression and mucin secretion in nasal epithelial cells. Acta Oto-Laryngologica, 122(6), 638-643. https://doi.org/10.1080/000164802320396321
Kim, Chang-Hoon ; Seob Song, K. ; Koo, J. S. ; Kim, H. U. ; Choi, J. Y. ; Kim, H. J. ; Yoon, J. H. / IL-13 suppresses MUC5AC gene expression and mucin secretion in nasal epithelial cells. In: Acta Oto-Laryngologica. 2002 ; Vol. 122, No. 6. pp. 638-643.
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abstract = "Recently, it was found that IL-13 is involved in allergic inflammation and mucus hypersecretion in in vivo animal models. However, the role of IL-13 in in vitro cellular models has yet to be determined. This study aimed to investigate the direct effect of IL-13 on mucin gene expression and mucin secretion in cultured normal human nasal epithelial cells. After treatment with IL-13, total mucin and MUC5AC mucin levels were measured using an immunoblotting assay. MUC2, MUC5AC and MUC8 mRNA expression were determined using reverse transcription-polymerase chain reaction. Also, immunostaining was performed using a MUC5AC antibody on histologic and cytospin slides. After treatment with ≥ 5 ng/ml IL-13, the level of total mucin and MUC5AC mucin secretion decreased substantially. The expression of MUC2 and MUC8 mRNA increased with higher concentrations of IL-13, but the expression of MUC5AC mRNA decreased. On the 7th day after IL-13 treatment, a significant decrease in the number of MUC5AC-positive cells was confirmed by immunostaining. These findings indicate that IL-13 suppresses MUC5AC mucin gene expression and mucin secretion in cultured normal human nasal epithelial cells in vitro.",
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Kim, C-H, Seob Song, K, Koo, JS, Kim, HU, Choi, JY, Kim, HJ & Yoon, JH 2002, 'IL-13 suppresses MUC5AC gene expression and mucin secretion in nasal epithelial cells', Acta Oto-Laryngologica, vol. 122, no. 6, pp. 638-643. https://doi.org/10.1080/000164802320396321

IL-13 suppresses MUC5AC gene expression and mucin secretion in nasal epithelial cells. / Kim, Chang-Hoon; Seob Song, K.; Koo, J. S.; Kim, H. U.; Choi, J. Y.; Kim, H. J.; Yoon, J. H.

In: Acta Oto-Laryngologica, Vol. 122, No. 6, 29.10.2002, p. 638-643.

Research output: Contribution to journalArticle

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