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2019 ; 80
(ä): 14-28
Nephropedia Template TP
gab.com Text
Twit Text FOAVip
Twit Text #
English Wikipedia
Defective lung function following influenza virus is due to prolonged, reversible
hyaluronan synthesis
#MMPMID29933044
Bell TJ
; Brand OJ
; Morgan DJ
; Salek-Ardakani S
; Jagger C
; Fujimori T
; Cholewa L
; Tilakaratna V
; Östling J
; Thomas M
; Day AJ
; Snelgrove RJ
; Hussell T
Matrix Biol
2019[Jul]; 80
(ä): 14-28
PMID29933044
show ga
Little is known about the impact of viral infections on lung matrix despite its
important contribution to mechanical stability and structural support. The
composition of matrix also indirectly controls inflammation by influencing cell
adhesion, migration, survival, proliferation and differentiation. Hyaluronan is a
significant component of the lung extracellular matrix and production and
degradation must be carefully balanced. We have discovered an imbalance in
hyaluronan production following resolution of a severe lung influenza virus
infection, driven by hyaluronan synthase 2 from epithelial cells, endothelial
cells and fibroblasts. Furthermore hyaluronan is complexed with inter-?-inhibitor
heavy chains due to elevated TNF-stimulated gene 6 expression and sequesters
CD44-expressing macrophages. We show that intranasal administration of exogenous
hyaluronidase is sufficient to release inter-?-inhibitor heavy chains, reduce
lung hyaluronan content and restore lung function. Hyaluronidase is already used
to facilitate dispersion of co-injected materials in the clinic. It is therefore
feasible that fibrotic changes following severe lung infection and inflammation
could be overcome by targeting abnormal matrix production.
|Alpha-Globulins/metabolism
[MESH]
|Animals
[MESH]
|Cell Adhesion Molecules/metabolism
[MESH]
|Endothelial Cells/metabolism
[MESH]
|Epithelial Cells/metabolism
[MESH]
|Female
[MESH]
|Fibroblasts/metabolism
[MESH]
|Humans
[MESH]
|Hyaluronan Receptors/metabolism
[MESH]
|Hyaluronan Synthases/*metabolism
[MESH]
|Hyaluronic Acid/*metabolism
[MESH]
|Influenza A Virus, H1N1 Subtype/*pathogenicity
[MESH]