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B Activation and Augmentation of IBß by Secretory Leukocyte Protease Inhibitor during Lung Inflammation
From the Department of Surgery,*
University of
Louisville School of Medicine, Louisville, Kentucky; the Departments of
Pathology and
Surgery,
University of Michigan Medical
School, Ann Arbor, Michigan; and the Department of Trauma
Surgery,§
University of Freiburg,
Freiburg/Breisgau, Germany
In earlier experiments, exogenous administration of
secretory leukocyte protease inhibitor (SLPI) suppressed acute lung
injury induced by deposition of IgG immune complexes. In the current
studies we examined the mechanism of the protective effects of SLPI in
this model. The presence of SLPI in the IgG immune complex-model of
lung injury reduced the increase in extravascular leakage of
125I-albumin, the intensity of up-regulation of
lung vascular intercellular adhesion molecule-1, and the
numbers of neutrophils accumulating in the lung. The presence of SLPI
caused greatly reduced activation (ie, nuclear translocation)
of the transcription nuclear factor-
B (NF-B) in lung cells but
did not suppress activation of lung mitogen-activated protein kinase.
SLPI did not alter NF-B activation in alveolar macrophages harvested
30 minutes after initiation of lung inflammation. In the presence of
SLPI, content of tumor necrosis factor-
, CXC
chemokines, and C5a in bronchoalveolar fluids was unaffected.
In the inflamed lungs, inhibition of NF-B activation by SLPI
was associated with elevated levels of lung IBß (but not IB)
protein in the absence of elevated mRNA for IBß. When instilled
into normal lung, SLPI also caused similar changes (increases)
in lung IBß. Finally, in the lung inflammatory model
used, the presence of anti-SLPI caused accentuated activation
of NF-B. These data confirm the anti-inflammatory effect of SLPI in
lung and point to a mechanism of anti-inflammatory effects of SLPI.
SLPI appears to function as an endogenous regulator of lung
inflammation.
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