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Molecular and Cellular Biology, December 1998, p. 7269-7277, Vol. 18, No. 12
Department of Molecular and Human
Genetics1 and
Department of
Pathology,2 Baylor College of Medicine,
Houston, Texas 77030
Received 20 May 1998/Returned for modification 15 July
1998/Accepted 14 September 1998
Members of the C/EBP (CCAAT/enhancer binding protein) family of
transcription factors play important roles in mediating the acute-phase
response (APR), an inflammatory process resulting from infection and/or
tissue damage. Among the C/EBP family of proteins, C/EBP
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C/EBP
Is Critical for the Neonatal
Acute-Phase Response to Inflammation
and -
were thought to be the primary mediators of the APR. The function of
C/EBP
in the APR has not been fully characterized to date. Here, we
investigate the role of C/EBP
in the APR by using neonatal mice that
lack C/EBP
expression. Northern blot analysis of acute-phase protein
gene expression in neonatal mice treated with purified bacterial
lipopolysaccharide or recombinant interleukin 1
as an inflammation
stimulus showed a strong APR in wild-type mice, but a response in
C/EBP
null animals was completely lacking. The C/EBP
knockout and
wild-type mice demonstrated elevations in C/EBP
and -
mRNA
expression and DNA binding as well as increased DNA binding of NF-
B,
all of which are known to be important in the APR. Null mice, however, failed to activate STAT3 binding in response to lipopolysaccharide. Our
results provide the first evidence that C/EBP
is absolutely required
for the APR in neonatal mice, is involved in STAT3 regulation, and
cannot be compensated for by other C/EBP family members.
*
Corresponding author. Mailing address: Department of
Pathology, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030. Phone: (713) 770-1868. Fax: (713) 770-1032. E-mail:
gretchen{at}bcm.tmc.edu.
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