PMID- 19718408
OWN - NLM
STAT- MEDLINE
DCOM- 20100303
LR  - 20211020
IS  - 1976-2437 (Electronic)
IS  - 0513-5796 (Print)
IS  - 0513-5796 (Linking)
VI  - 50
IP  - 4
DP  - 2009 Aug 31
TI  - The soluble tumor necrosis factor-alpha receptor suppresses airway inflammation 
      in a murine model of acute asthma.
PG  - 569-75
LID - 10.3349/ymj.2009.50.4.569 [doi]
AB  - PURPOSE: Tumor necrosis factor-alpha (TNF-alpha) is a proinflammatory cytokine 
      that has been implicated in many aspects of the airway pathology in asthma. 
      TNF-alpha blocking strategies are now being tried in asthma patients. This study 
      investigated whether TNF-alpha blocking therapy inhibits airway inflammation and 
      airway hyperresponsiveness (AHR) in a mouse model of asthma. We also evaluated 
      the effect of TNF-alpha blocking therapy on cytokine production and adhesion 
      molecule expression. MATERIALS AND METHODS: Ovalbumin (OVA) sensitized BALB/c 
      female mice were exposed to intranasal OVA administration on days 31, 33, 35, and 
      37. Mice were treated intraperitoneally with soluble TNF-alpha receptor (sTNFR) 
      during the OVA challenge. RESULTS: There were statistically significant decreases 
      in the numbers of total cell and eosinophil in bronchoalveolar lavage fluid 
      (BALF) in the sTNFR treated group compared with the OVA group. However, 
      sTNFR-treatment did not significantly decrease AHR. Anti-inflammatory effect of 
      sTNFR was accompanied with reduction of T helper 2 cytokine levels including 
      interleukin (IL)-4, IL-5 and IL-13 in BALF and vascular cell adhesion molecule 1 
      expression in lung tissue. CONCLUSION: These results suggest that sTNFR treatment 
      can suppress the airway inflammation via regulation of Th2 cytokine production 
      and adhesion molecule expression in bronchial asthma.
FAU - Nam, Hae-Seong
AU  - Nam HS
AD  - Division of Pulmonology, Department of Internal Medicine, College of Medicine, 
      The Catholic University of Korea, Seoul, Korea.
FAU - Lee, Sook Young
AU  - Lee SY
FAU - Kim, Seung Jun
AU  - Kim SJ
FAU - Kim, Ju Sang
AU  - Kim JS
FAU - Kwon, Soon Seog
AU  - Kwon SS
FAU - Kim, Young Kyoon
AU  - Kim YK
FAU - Kim, Kwan Hyung
AU  - Kim KH
FAU - Moon, Hwa Sik
AU  - Moon HS
FAU - Song, Jeong Sup
AU  - Song JS
FAU - Park, Sung Hak
AU  - Park SH
FAU - Kim, Seok Chan
AU  - Kim SC
LA  - eng
PT  - Journal Article
DEP - 20090819
PL  - Korea (South)
TA  - Yonsei Med J
JT  - Yonsei medical journal
JID - 0414003
RN  - 0 (Anti-Asthmatic Agents)
RN  - 0 (Interleukin-13)
RN  - 0 (Interleukin-5)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 207137-56-2 (Interleukin-4)
RN  - 9006-59-1 (Ovalbumin)
SB  - IM
MH  - Animals
MH  - Anti-Asthmatic Agents/*therapeutic use
MH  - Asthma/*drug therapy/*immunology
MH  - Blotting, Western
MH  - Bronchi/drug effects
MH  - Bronchial Hyperreactivity
MH  - Bronchoalveolar Lavage Fluid/immunology
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Female
MH  - Immunohistochemistry
MH  - Inflammation/*drug therapy
MH  - Interleukin-13/metabolism
MH  - Interleukin-4/metabolism
MH  - Interleukin-5/metabolism
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Ovalbumin/pharmacology
MH  - Tumor Necrosis Factor-alpha/*therapeutic use
PMC - PMC2730622
OTO - NOTNLM
OT  - Asthma
OT  - airway inflammation
OT  - soluble TNF-alpha receptor
COIS- The authors have no financial conflicts of interest.
EDAT- 2009/09/01 06:00
MHDA- 2010/03/04 06:00
PMCR- 2009/08/31
CRDT- 2009/09/01 09:00
PHST- 2008/10/24 00:00 [received]
PHST- 2009/01/15 00:00 [revised]
PHST- 2009/01/23 00:00 [accepted]
PHST- 2009/09/01 09:00 [entrez]
PHST- 2009/09/01 06:00 [pubmed]
PHST- 2010/03/04 06:00 [medline]
PHST- 2009/08/31 00:00 [pmc-release]
AID - 10.3349/ymj.2009.50.4.569 [doi]
PST - ppublish
SO  - Yonsei Med J. 2009 Aug 31;50(4):569-75. doi: 10.3349/ymj.2009.50.4.569. Epub 2009 
      Aug 19.