PMID- 10541330
OWN - NLM
STAT- MEDLINE
DCOM- 19991208
LR  - 20161124
IS  - 0031-3998 (Print)
IS  - 0031-3998 (Linking)
VI  - 46
IP  - 5
DP  - 1999 Nov
TI  - Antenatal dexamethasone suppresses tumor necrosis factor-alpha expression in 
      hypoplastic lung in nitrofen-induced diaphragmatic hernia in rats.
PG  - 633-7
AB  - The hypoplastic lung in congenital diaphragmatic hernia (CDH) has both a 
      quantitative and qualitative reduction in surfactant. Tumor necrosis factor-alpha 
      (TNF-alpha) drastically decreases surfactant phospholipids synthesis by isolated 
      human type II pneumocytes. Recently, it was shown that TNF-alpha mRNA expression 
      is increased in human hypoplastic CDH lung. Antenatal glucocorticoid therapy 
      demonstrates improved surfactant biochemical immaturity in an animal CDH model. 
      The aim of this study was to investigate the effect of antenatal dexamethasone 
      (Dex) on TNF-alpha protein and gene expression in nitrofen-induced CDH 
      hypoplastic lung in rats. A CDH model was induced in pregnant rats after the 
      administration of nitrofen on d 9.5 of gestation. Dex was given intraperitoneally 
      on d 18.5 and 19.5. Cesarean section was performed on d 21. In situ hybridization 
      was performed with a rat TNF-alpha-specific and digoxigenin-labeled 
      oligonucleotide probe. TNF-alpha level was measured in solubilized lung tissue 
      extracts by ELISA. In control lung, TNF-alpha mRNA expression was weak or absent. 
      In contrast, strong TNF-alpha mRNA expression was demonstrated in type II 
      pneumocytes and bronchiolar epithelium in CDH lung. In Dex-treated CDH lung, 
      TNF-alpha mRNA expression was weak in both type II pneumocytes and the 
      bronchiolar epithelium. The level of TNF-alpha was elevated significantly in CDH 
      lung compared with levels in control lung extracts (p < 0.01). In Dex-treated CDH 
      lung, TNF-alpha protein was significantly decreased compared with CDH lung (p < 
      0.05). Our findings suggest that the reduction in the local production of 
      TNF-alpha may be one contributing mechanism by which antenatal glucocorticoid 
      therapy improves pulmonary parenchymal immaturity, including surfactant.
FAU - Shima, H
AU  - Shima H
AD  - Children's Research Centre, Our Lady's Hospital for Sick Children, Dublin, 
      Ireland.
FAU - Ohshiro, K
AU  - Ohshiro K
FAU - Taira, Y
AU  - Taira Y
FAU - Miyazaki, E
AU  - Miyazaki E
FAU - Oue, T
AU  - Oue T
FAU - Puri, P
AU  - Puri P
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Pediatr Res
JT  - Pediatric research
JID - 0100714
RN  - 0 (Glucocorticoids)
RN  - 0 (Phenyl Ethers)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 7S5I7G3JQL (Dexamethasone)
RN  - N71UYG034A (nitrofen)
SB  - IM
MH  - Abnormalities, Drug-Induced/etiology/metabolism
MH  - Animals
MH  - Dexamethasone/*therapeutic use
MH  - Female
MH  - Fetal Diseases/chemically induced/*drug therapy/metabolism
MH  - Gene Expression Regulation, Neoplastic/drug effects
MH  - Glucocorticoids/*therapeutic use
MH  - Hernia, Diaphragmatic/chemically induced/*drug therapy/metabolism
MH  - In Situ Hybridization
MH  - Lung/*abnormalities
MH  - Phenyl Ethers/toxicity
MH  - Pregnancy
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Tumor Necrosis Factor-alpha/genetics/*metabolism
EDAT- 1999/12/14 00:00
MHDA- 1999/12/14 00:01
CRDT- 1999/12/14 00:00
PHST- 1999/12/14 00:00 [pubmed]
PHST- 1999/12/14 00:01 [medline]
PHST- 1999/12/14 00:00 [entrez]
AID - 10.1203/00006450-199911000-00023 [doi]
PST - ppublish
SO  - Pediatr Res. 1999 Nov;46(5):633-7. doi: 10.1203/00006450-199911000-00023.