Publication: Differential severity of LPS-induced lung injury in CD26/DPP4 positive and deficient F344 rats
Authors
Zientara, Alicja ; Stephan, Michael ; von Hörsten, Stephan ; Schmied, Andreas
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Description
Abstract
Background. Lipopolysaccharide (LPS)
induced inflammation often leads to lung injury, in
which pulmonary recruitment of neutrophils plays a
pivotal role. Inflammatory processes are influenced by
CD26/DPP4, highly expressed in lungs. Asthma induced
CD26/DPP4 deficient (CD26/DPP4 - ) Fischer (F) 344
rats suffering from a transport block in the rER caused
by a point mutation showed reduced pulmonary
inflammation and reduced expression of immuno-
modulating surfactant proteins (SP). The degree of LPS
induced lung injury in CD26/DPP4 deficient rats has not
been investigated so far.
Objective. We hypothesize that LPS induced lung
injury leads not only to an attenuated inflammation but
also to a reduced SP expression and decreased structural
damage in CD26/DPP4 - rats.
Methods. Both genotypes were intratracheally
instilled with 250 μl LPS or with 250 μl 0.9% NaCl.
Nine hours later animals were killed and either
bronchoalveolar lavage was carried out to determine
inflammatory cells and surface tension or lung blocks
were removed and processed for histology,
immunohistochemistry, electron microscopy or qRt-PCR
analyses and Western Blot analyses.
Results. Signs of acute lung injury, such as structural
damage of the blood gas barrier occurred only
sporadically in both genotypes. LPS-induced
CD26/DPP4 - rats showed decreased gene expression of
SP-A and SP-D and reduced signs of lung inflammation
associated with a reduced alveolar influx of
macrophages and neutrophils.
Conclusions. Less pulmonary inflammation
combined with less structural alterations and minor
expression of immunomodulating SP may be an
indication of the critical role of CD26/DPP4 in
regulating lung inflammation
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