Asian Sand Dust Upregulates IL-6 and IL-8 via ROS, JNK, ERK, and CREB Signaling in Human Nasal Fibroblasts

Hyun Woo Yang, Joo Hoo Park, Jae Min Shin, Heung Man Lee, Il Ho Park

Research output: Contribution to journalArticle

Abstract

Background: Asian sand dust (ASD) profoundly affects respiratory health by inducing inflammation and causing upper airway inflammatory diseases. Interleukin (IL)-6 and IL-8 are pro-inflammatory mediators that are involved in upper airway inflammatory diseases. However, the effect of ASD on the production of IL-6 and IL-8 in nasal fibroblasts has not been adequately studied. We investigated the effect of ASD on the induction of pro-inflammatory mediators and its underlying mechanisms in nasal fibroblasts. Methods: Real-time cytotoxicity assays were used to determine the effect of ASD on the viability of fibroblasts. Enzyme-linked immunosorbent assays and real-time polymerase chain reactions were performed to determine whether ASD induced the expression of IL-6 and IL-8. Reactive oxygen species (ROS) were quantified using 2, 7-dichlorofluorescein-diacetate and MitoSOX Red. Induction of IL-6 and IL-8 signal transduction pathways by ASD was confirmed by Western blotting. Ex vivo culture of the inferior turbinate tissue was performed to confirm the effects of ASD. Results: ASD upregulated ROS levels, and this in turn promoted IL-6 and IL-8 expression through the MAPK (JNK and ERK) and CREB signaling pathways in nasal fibroblasts. However, ASD did not induce phosphorylation of p38. Specific inhibitors of each pathway (ROS, JNK, ERK, and CREB inhibitors) suppressed ASD-induced IL-6 and IL-8 upregulation. Conclusions: ASD induces pro-inflammatory mediators, and the increased levels of IL-6 and IL-8 might be associated with the pathogenesis of chronic rhinosinusitis.

Original languageEnglish
JournalAmerican Journal of Rhinology and Allergy
DOIs
Publication statusAccepted/In press - 2019 Jan 1

Fingerprint

Dust
Interleukin-8
Nose
Interleukin-6
Reactive Oxygen Species
Up-Regulation
Fibroblasts
Turbinates
Real-Time Polymerase Chain Reaction
Signal Transduction
Western Blotting
Enzyme-Linked Immunosorbent Assay
Phosphorylation
Inflammation

Keywords

  • Asian sand dust
  • chronic rhinosinusitis
  • interleukin 6
  • interleukin 8
  • nasal fibroblast
  • reactive oxygen species

ASJC Scopus subject areas

  • Immunology and Allergy
  • Otorhinolaryngology

Cite this

Asian Sand Dust Upregulates IL-6 and IL-8 via ROS, JNK, ERK, and CREB Signaling in Human Nasal Fibroblasts. / Yang, Hyun Woo; Park, Joo Hoo; Shin, Jae Min; Lee, Heung Man; Park, Il Ho.

In: American Journal of Rhinology and Allergy, 01.01.2019.

Research output: Contribution to journalArticle

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AB - Background: Asian sand dust (ASD) profoundly affects respiratory health by inducing inflammation and causing upper airway inflammatory diseases. Interleukin (IL)-6 and IL-8 are pro-inflammatory mediators that are involved in upper airway inflammatory diseases. However, the effect of ASD on the production of IL-6 and IL-8 in nasal fibroblasts has not been adequately studied. We investigated the effect of ASD on the induction of pro-inflammatory mediators and its underlying mechanisms in nasal fibroblasts. Methods: Real-time cytotoxicity assays were used to determine the effect of ASD on the viability of fibroblasts. Enzyme-linked immunosorbent assays and real-time polymerase chain reactions were performed to determine whether ASD induced the expression of IL-6 and IL-8. Reactive oxygen species (ROS) were quantified using 2, 7-dichlorofluorescein-diacetate and MitoSOX Red. Induction of IL-6 and IL-8 signal transduction pathways by ASD was confirmed by Western blotting. Ex vivo culture of the inferior turbinate tissue was performed to confirm the effects of ASD. Results: ASD upregulated ROS levels, and this in turn promoted IL-6 and IL-8 expression through the MAPK (JNK and ERK) and CREB signaling pathways in nasal fibroblasts. However, ASD did not induce phosphorylation of p38. Specific inhibitors of each pathway (ROS, JNK, ERK, and CREB inhibitors) suppressed ASD-induced IL-6 and IL-8 upregulation. Conclusions: ASD induces pro-inflammatory mediators, and the increased levels of IL-6 and IL-8 might be associated with the pathogenesis of chronic rhinosinusitis.

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