Zerumbone enhances the Th1 response and ameliorates ovalbumin-induced Th2 responses and airway inflammation in mice

Shieh, Ying Hua; Huang, Huei Mei; Wang, Ching Chiung; Lee, Chen Chen; Fan, Chia Kwung; Lee, Yueh Lun

doi:10.1016/j.intimp.2014.12.027

Cited by 55 publications

(33 citation statements)

References 37 publications

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“…Moreover, histamine induced 6,15 Th2 cell responses initiate the pathogenesis of asthma through the productions of Th2 cytokines. 16 Esculetin reduces the percentage of Th17 cells in asthmatic mouse, and suppresses the production of Th2 and Th17-related cytokines including IL-4, IL-5, IL-13, and IL-17A. 6 These findings suggest that esculetin possess anti-allergic and anti-inflammatory effects.…”

Section: Discussionmentioning

confidence: 99%

“…Th17 cells are marked by the generations of various cytokines, and it has been observed to be involved in tissue pathology in several autoimmune disorders including allergic asthma . Th2 cell responses initiate the pathogenesis of asthma through the productions of Th2 cytokines . Esculetin reduces the percentage of Th17 cells in asthmatic mouse, and suppresses the production of Th2 and Th17‐related cytokines including IL‐4, IL‐5, IL‐13, and IL‐17A .…”

Section: Discussionmentioning

confidence: 99%

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Esculetin inhibits histamine‐induced expression of inflammatory cytokines and mucin in nasal epithelial cells

Sun

Wang

2019

Clin Exp Pharma Physio

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Allergic rhinitis (AR) is a type of respiratory disease closely associated with chronic inflammation. Esculetin is a natural coumarin derivative and has been reported to possess anti‐allergic and anti‐inflammatory effects. However, the roles of esculetin in AR have not been studied. In this study, we aimed to examine the effect of esculetin on AR using an in vitro model. The human nasal epithelial cells (HNEpC) were stimulated by histamine for 24 hours with or without the pretreatment of esculetin. The mRNA levels and production of inflammatory cytokines including IL‐6 and IL‐8, as well as mucin 5AC (MUC5AC) were measured using qRT‐PCR and ELISA, respectively. The results showed that esculetin suppressed histamine‐induced expression and secretion of IL‐6, IL‐8, and MUC5AC in HNEpCs. Furthermore, we examined the effect of esculetin on NF‐κB pathway by detecting the expression levels of NF‐κB p65, p‐p65 and IκBα using western blot analysis. Esculetin treatment suppressed the histamine‐induced p‐p65 expression and p‐IκBα degradation. Inhibiting NF‐κB pathway suppressed histamine‐induced production of IL‐6, IL‐8, and MUC5AC in HNEpCs. These findings suggested that esculetin suppressed histamine‐induced production of inflammatory cytokines and mucin in HNEpCs, which were partly mediated by the inhibition of NF‐κB pathway.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Esculetin inhibits histamine‐induced expression of inflammatory cytokines and mucin in nasal epithelial cells

Sun

Wang

2019

Clin Exp Pharma Physio

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“…The existing literature already reported some examples of antioxidant therapy for the pulmonary toxicities (251). Zerumbone, an antioxidant, attenuated Th2 responses induced by ovalbumin and decreased airway inflammation in a mice model of study (252). Similarly, naringin, a flavinoid antioxidant, also attenuated airway inflammation in a mouse model of asthma (253).…”

Section: Possible Therapeutic Interventions To Combat Soot- or Cb-assmentioning

confidence: 99%

The Toxicological Mechanisms of Environmental Soot (Black Carbon) and Carbon Black: Focus on Oxidative Stress and Inflammatory Pathways

2017

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The environmental soot and carbon blacks (CBs) cause many diseases in humans, but their underlying mechanisms of toxicity are still poorly understood. Both are formed after the incomplete combustion of hydrocarbons but differ in their constituents and percent carbon contents. For the first time, “Sir Percival Pott” described soot as a carcinogen, which was subsequently confirmed by many others. The existing data suggest three main types of diseases due to soot and CB exposures: cancer, respiratory diseases, and cardiovascular dysfunctions. Experimental models revealed the involvement of oxidative stress, DNA methylation, formation of DNA adducts, and Aryl hydrocarbon receptor activation as the key mechanisms of soot- and CB-induced cancers. Metals including Si, Fe, Mn, Ti, and Co in soot also contribute in the reactive oxygen species (ROS)-mediated DNA damage. Mechanistically, ROS-induced DNA damage is further enhanced by eosinophils and neutrophils via halide (Cl− and Br−) dependent DNA adducts formation. The activation of pulmonary dendritic cells, T helper type 2 cells, and mast cells is crucial mediators in the pathology of soot- or CB-induced respiratory disease. Polyunsaturated fatty acids (PUFAs) were also found to modulate T cells functions in respiratory diseases. Particularly, telomerase reverse transcriptase was found to play the critical role in soot- and CB-induced cardiovascular dysfunctions. In this review, we propose integrated mechanisms of soot- and CB-induced toxicity emphasizing the role of inflammatory mediators and oxidative stress. We also suggest use of antioxidants and PUFAs as protective strategies against soot- and CB-induced disorders.

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“…The ovalbumin-induced airway inflammation in BALB/c mice has been widely used as an experimental model of asthma been mediated by TH 1 [60,61], TH 2 , and TH 17 [62] cells and induces eosinophil and neutrophil recruitment, goblet cell hyperplasia, increased mucus production, and airway obstruction [63][64][65].…”

Section: Introductionmentioning

confidence: 99%

Hyperoxia promotes polarization of the immune response in ovalbumin‐induced airway inflammation, leading to a TH₁₇ cell phenotype

Nagato

Bezerra²,

Talvani

et al. 2015

Immunity Inflam & Disease

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Previous studies have demonstrated that hyperoxia-induced stress and oxidative damage to the lungs of mice lead to an increase in IL-6, TNF-α, and TGF-β expression. Together, IL-6 and TGF-β have been known to direct T cell differentiation toward the TH17 phenotype. In the current study, we tested the hypothesis that hyperoxia promotes the polarization of T cells to the TH17 cell phenotype in response to ovalbumin-induced acute airway inflammation. Airway inflammation was induced in female BALB/c mice by intraperitoneal sensitization and intranasal introduction of ovalbumin, followed by challenge methacholine. After the methacholine challenge, animals were exposed to hyperoxic conditions in an inhalation chamber for 24 h. The controls were subjected to normoxia or aluminum hydroxide dissolved in phosphate buffered saline. After 24 h of hyperoxia, the number of macrophages and lymphocytes decreased in animals with ovalbumin-induced airway inflammation, whereas the number of neutrophils increased after ovalbumin-induced airway inflammation. The results showed that expression of Nrf2, iNOS, T-bet and IL-17 increased after 24 of hyperoxia in both alveolar macrophages and in lung epithelial cells, compared with both animals that remained in room air, and animals with ovalbumin-induced airway inflammation. Hyperoxia alone without the induction of airway inflammation lead to increased levels of TNF-α and CCL5, whereas hyperoxia after inflammation lead to decreased CCL2 levels. Histological evidence of extravasation of inflammatory cells into the perivascular and peribronchial regions of the lungs was observed after pulmonary inflammation and hyperoxia. Hyperoxia promotes polarization of the immune response toward the TH17 phenotype, resulting in tissue damage associated with oxidative stress, and the migration of neutrophils to the lung and airways. Elucidating the effect of hyperoxia on ovalbumin-induced acute airway inflammation is relevant to preventing or treating asthmatic patients that require oxygen supplementation to reverse the hypoxemia.

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Zerumbone enhances the Th1 response and ameliorates ovalbumin-induced Th2 responses and airway inflammation in mice

Cited by 55 publications

References 37 publications

Esculetin inhibits histamine‐induced expression of inflammatory cytokines and mucin in nasal epithelial cells

Esculetin inhibits histamine‐induced expression of inflammatory cytokines and mucin in nasal epithelial cells

The Toxicological Mechanisms of Environmental Soot (Black Carbon) and Carbon Black: Focus on Oxidative Stress and Inflammatory Pathways

Hyperoxia promotes polarization of the immune response in ovalbumin‐induced airway inflammation, leading to a TH₁₇ cell phenotype

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Zerumbone enhances the Th1 response and ameliorates ovalbumin-induced Th2 responses and airway inflammation in mice

Cited by 55 publications

References 37 publications

Esculetin inhibits histamine‐induced expression of inflammatory cytokines and mucin in nasal epithelial cells

Esculetin inhibits histamine‐induced expression of inflammatory cytokines and mucin in nasal epithelial cells

The Toxicological Mechanisms of Environmental Soot (Black Carbon) and Carbon Black: Focus on Oxidative Stress and Inflammatory Pathways

Hyperoxia promotes polarization of the immune response in ovalbumin‐induced airway inflammation, leading to a TH17 cell phenotype

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Product

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About

Hyperoxia promotes polarization of the immune response in ovalbumin‐induced airway inflammation, leading to a TH₁₇ cell phenotype