PMID- 12781029
OWN - NLM
STAT- MEDLINE
DCOM- 20030710
LR  - 20081121
IS  - 0366-6999 (Print)
IS  - 0366-6999 (Linking)
VI  - 116
IP  - 3
DP  - 2003 Mar
TI  - Effects of interleukin-18 on asthmatic airway inflammation and nuclear factor 
      kappa-B in murine models.
PG  - 323-7
AB  - OBJECTIVE: To investigate the effects of Interleukin-18 (IL-18) on asthmatic 
      airway inflammation and nuclear factor kappa-B (NF-kappaB) in a murine asthmatic 
      model. METHODS: BALB/C mice were randomly divided into three groups: group A 
      (control group, n = 10); group B (asthmatic model group, n = 10); group C (IL-18 
      injection group, n = 10). The asthmatic model was established in group B and C by 
      respiratory syncytial virus (RSV) killed by ultraviolet light. Saline solution 
      (0.1 ml) and IL-18 (0.1 ml, 1 micro g) was injected in groups B and C at seven 
      time points (1, 2, 7, 8, 9, 21, 22 d). The symptoms and the numbers of 
      eosinophils and plasmacytes in the airways were observed and the expression of 
      NF-kappaB activation in the lung was analyzed by immunohistochemistry (IHC) and 
      Western blot. RESULTS: The symptoms of group C were more severe than in groups A 
      and B. Group A did not have EOS and plasmacytes in the airway submucosal while 
      the numbers of eosinophils [15 +/- 3 (average cell counts per microscopic visual 
      field, the same below)] and plasmacytes (10 +/- 2) in group B were found to have 
      increased significantly. But the numbers of eosinophils and plasmacytes in group 
      C were decreased significantly when compared with group B (6 +/- 2 and 2 +/- 1, 
      respectively, both P < 0.05). ISH showed that the expression of NF-kappaB 
      activation in group B was stronger than that in groups A and C. The amount of 
      NF-kappaB inhibitor (IkappaB) in group A and group C were 3.5 times and 2.5 times 
      more than that of group B respectively via Western blot. CONCLUSION: IL-18 can 
      inhibit asthmatic airway inflammation in mice and its mechanism may be due to the 
      fact that IL-18 can inhibit the activation of NF-kappaB in the murine asthmatic 
      model.
FAU - Zhang, Huilan
AU  - Zhang H
AD  - Department of Respiratory Diseases, Tongji Hospital, Tongji Medical School, 
      Huazhong University of Science and Technology, Wuhan 430030, China. 
      huilanz_76@163.com
FAU - Zhang, Zhenxiang
AU  - Zhang Z
FAU - Xu, Yongjian
AU  - Xu Y
LA  - eng
PT  - Journal Article
PL  - China
TA  - Chin Med J (Engl)
JT  - Chinese medical journal
JID - 7513795
RN  - 0 (Interleukin-18)
RN  - 0 (NF-kappa B)
RN  - 37341-29-0 (Immunoglobulin E)
RN  - 82115-62-6 (Interferon-gamma)
SB  - IM
MH  - Animals
MH  - Asthma/*therapy
MH  - Blotting, Western
MH  - Disease Models, Animal
MH  - Female
MH  - Immunoglobulin E/biosynthesis
MH  - Immunohistochemistry
MH  - Interferon-gamma/physiology
MH  - Interleukin-18/genetics/pharmacology/*therapeutic use
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - NF-kappa B/*antagonists & inhibitors
EDAT- 2003/06/05 05:00
MHDA- 2003/07/11 05:00
CRDT- 2003/06/05 05:00
PHST- 2003/06/05 05:00 [pubmed]
PHST- 2003/07/11 05:00 [medline]
PHST- 2003/06/05 05:00 [entrez]
PST - ppublish
SO  - Chin Med J (Engl). 2003 Mar;116(3):323-7.