Antioxidant Down-Regulates Interleukin-18 Expression in Asthma

@article{Lee2006AntioxidantDI,
  title={Antioxidant Down-Regulates Interleukin-18 Expression in Asthma},
  author={Kyung Sun Lee and So Ri Kim and Seoung Ju Park and Kyung Hoon Min and Ka Young Lee and Sun Mi Jin and Wan-Hee Yoo and Yong Chul Lee},
  journal={Molecular Pharmacology},
  year={2006},
  volume={70},
  pages={1184 - 1193}
}
An alteration in the balance between a T-helper type 2 cell (Th2) response and a Th1 response may predispose to the development of bronchial asthma. Interleukin-18 (IL-18) has an ability to promote both Th1 and Th2 responses, depending on the surrounding cytokine environment. Reactive oxygen species (ROS) play a crucial role in the pathogenesis of airway inflammation and hyperresponsiveness. Recent studies have demonstrated that antioxidants are able to reduce airway inflammation and… 
View on ASPET
molpharm.aspetjournals.org
50 Citations
Highly Influential Citations
1
Background Citations
14
Methods Citations
4
Results Citations
3

50 Citations

Citation Type

Citation Type

Administration of vitamin E attenuates airway inflammation through restoration of Nrf2 in a mouse model of asthma
TLDR
Vitamin E treatment may have the therapeutic potential through restoration of the Nrf2 level, especially in elderly asthma, as assessed using an eosinophilic asthma model.
Serum Interleukin-18 Expression in Children With Bronchial Asthma
TLDR
Serum IL-18 was found underexpressed in a group of asthmatic children especially during exacerbation and further studies are needed to outline its exact role in the pathogenesis of asthma.
Mitochondrial Dysfunction and Oxidative Stress in Asthma: Implications for Mitochondria-Targeted Antioxidant Therapeutics
  • P. Reddy
  • Biology, Medicine
    Pharmaceuticals
  • 2011
TLDR
This article summarizes the latest research findings on the involvement of inflammatory changes, and mitochondrial dysfunction/oxidative stress in the development and progression of asthma, and the relationship between aging and age-related immunity in triggering asthma, the antioxidant therapeutic strategies in treating people with asthma.
L-2-Oxothiazolidine-4-Carboxylic Acid or α-Lipoic Acid Attenuates Airway Remodeling: Involvement of Nuclear Factor-κB (NF-κB), Nuclear Factor Erythroid 2p45-Related Factor-2 (Nrf2), and Hypoxia-Inducible Factor (HIF)
TLDR
It is demonstrated that OTC and LA can inhibit activation of NF-κB, Nrf2, and HIF, leading to attenuate allergen-induced airway remodeling, and down-regulated phosphoinositide 3-kinase activity and decreased phosphorylation of p38 mitogen-activated protein kinase but not extracellular signal-regulated kinase 1/2 or c-Jun N-terminal kinase.
Beneficial effects of high dose of L-arginine on airway hyperresponsiveness and airway inflammation in a murine model of asthma.
Interleukin-18: a pro-inflammatory cytokine that plays an important role in acute pancreatitis
TLDR
The use ofIL-18 antagonists as direct routes to block IL-18 activity and P2X7 receptor antagonists and interleukin-1β-converting enzyme (ICE) inhibitors as indirect routes to blocks IL-16 activity suggest that specific therapeutic inhibition of IL- 18 is a promising therapeutic approach for acute pancreatitis.
Glutathione redox control of asthma: from molecular mechanisms to therapeutic opportunities.
TLDR
Disruptions of redox signaling and control in asthma are discussed with a focus on the thiol, glutathione, and reduced (thiol) form (GSH).
IL-18 in induced sputum and airway hyperresponsiveness in mild asthmatics: effect of smoking.
Transforming growth factor β and severe asthma: a perfect storm.
Interleukin‐18‐deficient mice exhibit diminished chronic inflammation and airway remodelling in ovalbumin‐induced asthma model
TLDR
It is suggested that IL‐18 may enhance chronic airway inflammation and airway remodelling through the production of IFN‐γ, IL‐13 and TGF‐β1 in the OVA‐induced asthma mouse model.
...
1
2
3
4
5
...

References

SHOWING 1-10 OF 71 REFERENCES
IL-18 deficiency selectively enhances allergen-induced eosinophilia in mice.
Prevention of Th2-like cell responses by coadministration of IL-12 and IL-18 is associated with inhibition of antigen-induced airway hyperresponsiveness, eosinophilia, and serum IgE levels.
TLDR
Data show that, in vivo, the synergistic action of IL-12 and IL-18 is necessary to prevent Th2-like cell differentiation, and consequently inhibits the development of airway symptoms in a mouse model of allergic asthma.
Blockade of airway hyperresponsiveness and inflammation in a murine model of asthma by a prodrug of cysteine, L‐2‐ oxothiazolidine‐4‐carboxylic acid
  • Yong Chul Lee, K. Lee, +7 authors U. Kim
  • Biology, Medicine
    FASEB journal : official publication of the Federation of American Societies for Experimental Biology
  • 2004
TLDR
It is shown that the increased NF‐κB levels in nuclear protein extracts of lung tissues at 72 h after OVA inhalation were decreased by the administration of OTC, suggesting that OTC may reduce airway inflammation and hyper‐responsiveness through regulation of NF‐ KakB activity.
Differential Roles of IL-18 in Allergic Airway Disease: Induction of Eotaxin by Resident Cell Populations Exacerbates Eosinophil Accumulation1
TLDR
Data demonstrate that IL-18 may have multiple functions during an immune response that differ depending upon the local or systemic effects, and that neutralization ofIL-18 exacerbated, whereas exogenous IL- 18 had no effect on airway hyperreactivity.
A Small Molecule Inhibitor of Redox-Regulated NF-κB and Activator Protein-1 Transcription Blocks Allergic Airway Inflammation in a Mouse Asthma Model1
TLDR
Results support redox-regulated transcription as a therapeutic target in asthma and demonstrate that selective inhibitors can reduce allergic airway inflammation and AHR.
α-Lipoic acid inhibits airway inflammation and hyperresponsiveness in a mouse model of asthma
Airway epithelium expresses interleukin-18.
TLDR
The expression of interleukin-18 within airway epithelium and the regulation of this cytokine under conditions of both T-helper1 and T- Helper2 cytokine production are demonstrated.
alpha-Lipoic acid inhibits airway inflammation and hyperresponsiveness in a mouse model of asthma.
TLDR
It is suggested that oxidative stress plays an important role in asthmatic airway inflammation and that alpha-lipoic acid may be useful as adjuvant therapy for bronchial asthma.
Interleukin-18 regulates both Th1 and Th2 responses.
TLDR
IL-18 is a potent proinflammatory cytokine that has pathophysiological roles in several inflammatory conditions, and in principle, IL-18 enhances the IL-12-driven Th1 immune responses, but it can also stimulate Th2 immune responses in the absence of IL- 12.
IL-18 might reflect disease activity in mild and moderate asthma exacerbation.
TLDR
It was suggested that IL-18 may play a potential role to activate immunologic responses and may reflect disease activity in mild and moderate asthma exacerbation.
...
1
2
3
4
5
...