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Differential regulation of stem cell factor mRNA expression in human
endothelial cells by bacterial pathogens: an in vitro model of inflammation
A Koenig, E Yakisan, M Reuter, M Huang, KW Sykora, S Corbacioglu and K Welte
Department of Pediatric Hematology and Oncology, Children's Hospital,
Medical School Hannover, Germany.
Production of hematopoietic growth factors by endothelial cells plays a
pivotal role during inflammatory processes. Stem cell factor (SCF) is known
to be expressed constitutively in endothelial cells. To investigate the
regulation of this cytokine expression by inflammatory stimuli, we
cocultured human umbilical vein endothelial cells (HUVEC) with various
gram-negative bacterial strains (Escherichia coli, Yersinia enterocolitica,
Chlamydia trachomatis, and Neisseria meningitidis, respectively).
Experiments were performed with bacterial concentrations ranging from 10(2)
to 10(7) bacteria/mL for 3 hours. SCF- specific mRNA expression was studied
using Northern blot analysis. Stimulation with the enteropathogenic
bacterial strains Y enterocolitica and E coli resulted in a significant
concentration- dependent increase of SCF mRNA expression. Similar results
were obtained in coculture experiments with N meningitidis. As shown in
experiments with E coli, the accumulation of SCF transcripts was also
time-dependent. In contrast, coculture of HUVEC with the intracellular
gram-negative strain C trachomatis had no effect on SCF mRNA expression. To
elucidate the role of the gram-negative bacterial cell wall components, we
stimulated HUVEC with bacterial lipopolysaccharide (LPS). LPS induced a
maximal SCF mRNA accumulation within 2 hours followed by decrease of
SCF-specific transcripts to the basal level after 24 hours. In addition, we
exposed HUVEC to the classical inflammatory cytokine interleukin-1 alpha
(IL-1 alpha). Kinetic experiments showed a similar pattern of regulation
with an increase of SCF mRNA within 2 hours, persisting up to 12 hours, and
a decrease to basal transcription after 24 hours. From these data, we
conclude that SCF expression is regulated by inflammatory stimuli, such as
IL-1 alpha and bacterial pathogens, suggesting an important role of SCF
during inflammation.
Volume 83,
Issue 10,
pp. 2836-2843,
05/15/1994
Copyright © 1994 by The American Society of Hematology
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