PMID- 16822930
OWN - NLM
STAT- MEDLINE
DCOM- 20061129
LR  - 20131121
IS  - 0026-895X (Print)
IS  - 0026-895X (Linking)
VI  - 70
IP  - 4
DP  - 2006 Oct
TI  - Antioxidant down-regulates interleukin-18 expression in asthma.
PG  - 1184-93
AB  - 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 hyperreactivity in animal models of asthma. In 
      this study, we used a C57BL/6 mouse model of allergic asthma to examine the 
      effects of antioxidants on the regulation of IL-18 expression. Our present study 
      with ovalbumin-induced murine model of asthma revealed that ROS production in 
      cells from bronchoalveolar lavage fluids was increased and that administration of 
      L-2-oxothiazolidine-4-carboxylic acid or alpha-lipoic acid reduced the increased 
      levels of ROS, the increased expression of IL-18 protein and mRNA, airway 
      inflammation, and bronchial hyperresponsiveness. Our results also showed that 
      antioxidants down-regulated a transcription factor, nuclear factor-kappaB 
      (NF-kappaB), activity. These results indicate that antioxidants may reduce IL-18 
      expression in asthma by inhibiting the activity of NF-kappaB and suggest that ROS 
      regulate the IL-18 expression.
FAU - Lee, Kyung Sun
AU  - Lee KS
AD  - Department of Internal Medicine, Chonbuk National University Medical School, San 
      2-20, Geumamdong, Deokjin-gu, Jeonju, Jeonbuk 561-180, South Korea.
FAU - Kim, So Ri
AU  - Kim SR
FAU - Park, Seoung Ju
AU  - Park SJ
FAU - Min, Kyung Hoon
AU  - Min KH
FAU - Lee, Ka Young
AU  - Lee KY
FAU - Jin, Sun Mi
AU  - Jin SM
FAU - Yoo, Wan Hee
AU  - Yoo WH
FAU - Lee, Yong Chul
AU  - Lee YC
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20060705
PL  - United States
TA  - Mol Pharmacol
JT  - Molecular pharmacology
JID - 0035623
RN  - 0 (Antioxidants)
RN  - 0 (Interleukin-18)
RN  - 0 (Interleukins)
RN  - 0 (RNA, Messenger)
RN  - 0 (Reactive Oxygen Species)
RN  - 0 (Transcription Factor RelA)
RN  - 37341-29-0 (Immunoglobulin E)
RN  - 73Y7P0K73Y (Thioctic Acid)
RN  - 9006-59-1 (Ovalbumin)
RN  - GAN16C9B8O (Glutathione)
RN  - ULW86O013H (Glutathione Disulfide)
SB  - IM
MH  - Animals
MH  - Antioxidants/*pharmacology
MH  - Asthma/chemically induced/*metabolism/physiopathology
MH  - Bronchial Hyperreactivity/drug therapy
MH  - Bronchoalveolar Lavage Fluid/chemistry
MH  - Down-Regulation
MH  - Female
MH  - Glutathione/metabolism
MH  - Glutathione Disulfide/metabolism
MH  - Immunoglobulin E/blood/metabolism
MH  - Interleukin-18/*metabolism
MH  - Interleukins/metabolism
MH  - Lung/metabolism
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Ovalbumin
MH  - RNA, Messenger/*metabolism
MH  - Reactive Oxygen Species/metabolism
MH  - Thioctic Acid/pharmacology
MH  - Transcription Factor RelA/antagonists & inhibitors/metabolism
EDAT- 2006/07/11 09:00
MHDA- 2006/12/09 09:00
CRDT- 2006/07/11 09:00
PHST- 2006/07/11 09:00 [pubmed]
PHST- 2006/12/09 09:00 [medline]
PHST- 2006/07/11 09:00 [entrez]
AID - mol.106.024737 [pii]
AID - 10.1124/mol.106.024737 [doi]
PST - ppublish
SO  - Mol Pharmacol. 2006 Oct;70(4):1184-93. doi: 10.1124/mol.106.024737. Epub 2006 Jul 
      5.