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From the Department of Traumatology,*
University of
Freiburg, Freiburg, Germany; Sumitomo Pharmaceuticals Research
Center,
Osaka, Japan; and Department of
Pathology,
University of Michigan, Ann
Arbor, Michigan
Using two models of acute lung inflammatory injury in rats
(intrapulmonary deposition of immunoglobulin G immune complexes and
systemic activation of complement after infusion of purified cobra
venom factor), we have analyzed the requirements and patterns
for upregulation of lung vascular P-selectin. In the immune complex
model, upregulation of P-selectin was defined by Northern and
Western blot analysis of lung homogenates, by immunostaining of
lung tissue, and by vascular fixation of
125I-labeled anti-P-selectin. P-selectin protein was
detected by 1 hour (long before detection of mRNA) and expression was
sustained for the next 7 hours, in striking contrast to the
pattern of P-selectin expression in the cobra venom factor
model, in which upregulation was very transient (within the 1st
hour). In the immune complex model, injury and neutrophil
accumulation were P-selectin dependent. Upregulation of P-selectin was
dependent on an intact complement system, and the presence of
blood neutrophils was susceptible to the antioxidant dimethyl sulfoxide
and required C5a but not tumor necrosis factor 
. In
contrast, in the cobra venom factor model, upregulation
of P-selectin, which is C5a dependent, was also
dimethyl sulfoxide sensitive but neutrophil independent.
Different mechanisms that may explain why upregulation of lung
vascular P-selectin is either transient or sustained are
discussed.
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