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2017 ; 95
(5
): 461-472
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S100A8/A9 and S100A9 reduce acute lung injury
#MMPMID28074060
Hiroshima Y
; Hsu K
; Tedla N
; Wong SW
; Chow S
; Kawaguchi N
; Geczy CL
Immunol Cell Biol
2017[May]; 95
(5
): 461-472
PMID28074060
show ga
S100A8 and S100A9 are myeloid cell-derived proteins that are elevated in several
types of inflammatory lung disorders. Pro- and anti-inflammatory properties are
reported and these proteins are proposed to activate TLR4. S100A8 and S100A9 can
function separately, likely through distinct receptors but a systematic
comparison of their effects in vivo are limited. Here we assess inflammation in
murine lung following S100A9 and S100A8/A9 inhalation. Unlike S100A8, S100A9
promoted mild neutrophil and lymphocyte influx, possibly mediated in part, by
increased mast cell degranulation and selective upregulation of some chemokine
genes, particularly CXCL-10. S100 proteins did not significantly induce
proinflammatory mediators including TNF-?, interleukin-1? (IL-1?), IL-6 or serum
amyloid A3 (SAA3). In contrast to S100A8, neither preparation induced S100A8 or
IL-10 mRNA/protein in airway epithelial cells, or in tracheal epithelial cells in
vitro. Like S100A8, S100A9 and S100A8/A9 reduced neutrophil influx in acute lung
injury provoked by lipopolysaccharide (LPS) challenge but were somewhat less
inhibitory, possibly because of differential effects on expression of some
chemokines, IL-1?, SAA3 and IL-10. Novel common pathways including increased
induction of an NAD(+)-dependent protein deacetylase sirtuin-1 that may reduce
NF-?B signalling, and increased STAT3 activation may reduce LPS activation.
Results suggest a role for these proteins in normal homeostasis and protective
mechanisms in the lung.