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Blood, Vol. 93 No. 9 (May 1), 1999:
pp. 3096-3105
CCAAT/Enhancer Binding Protein  Is Critical for Effective
Neutrophil-Mediated Response to Inflammatory Challenge
Julie Lekstrom-Himes and
Kleanthis G. Xanthopoulos
From the Clinical Gene Therapy Branch, National Human Genome Research
Institute, National Institutes of Health, Bethesda, MD.
Targeted mutation of CCAAT/enhancer binding protein
(C/EBP)  in mice results in early death, primarily due to
spontaneous infection with Pseudomonas aeruginosa. Functional
analysis of C/EBP-deficient neutrophils, in an in vivo model of
peritoneal inflammation, shows multiple defects. Reduction of
phagocytotic killing by C/EBP-deficient neutrophils is a result of
decreased uptake of opsonized bacteria as well as little to no
expression of secondary granule proteins. Abnormalities in neutrophil
migration detected in a chemical peritonitis model are likely secondary to abnormal CD11b integrin and L-selectin expression on
C/EBP-deficient neutrophils. Alterations in neutrophil cytokine
expression in response to inflammation show decreased levels of
interleukin-1 receptor antagonist (IL-1Ra) and increased levels of
tumor necrosis factor- (TNF-) expression by C/EBP-deficient
neutrophils. Additionally, TNF- expression is increased in
nonactivated, circulating C/EBP-deficient neutrophils. Overall,
C/EBP-deficient neutrophils are severely functionally impaired,
evoking an abnormal microenvironment, which may contribute to the loss
of normal responses to inflammatory stimuli. Similarities between the
C/EBP-deficient mouse model and the human disease, specific granule
deficiency, will be discussed.
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