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2019 ; 14
(10
): e0223430
Nephropedia Template TP
Huang S
; Goplen NP
; Zhu B
; Cheon IS
; Son Y
; Wang Z
; Li C
; Dai Q
; Jiang L
; Xiang M
; Carmona EM
; Vassallo R
; Limper AH
; Sun J
PLoS One
2019[]; 14
(10
): e0223430
PMID31584978
show ga
Influenza virus causes a heterogeneous respiratory infectious disease ranging
from self-limiting symptoms to non-resolving pathology in the lungs. Worldwide,
seasonal influenza infections claim ~500,000 lives annually. Recent reports
describe pathologic pulmonary sequelae that result in remodeling the architecture
of lung parenchyma following respiratory infections. These dysfunctional recovery
processes that disproportionately impact the elderly have been understudied.
Macrophages are involved in tissue remodeling and are critical for survival of
severe influenza infection. Here, we found intrinsic deficiency of the nuclear
receptor PPAR-? in myeloid cells delayed the resolution of pulmonary inflammation
following influenza infection. Mice with myeloid cell-specific PPAR-? deficiency
subsequently presented with increased influenza-induced deposition of pulmonary
collagen compared to control mice. This dysfunctional lung remodeling was
progressive and sustained for at least 3 months following infection of mice with
myeloid PPAR-? deficiency. These progressive changes were accompanied by a
pro-fibrotic gene signature from lung macrophages and preceded by deficiencies in
activation of genes involved with damage repair. Importantly similar aberrant
gene expression patterns were also found in a secondary analysis of a study where
macrophages were isolated from patients with fibrotic interstitial lung disease.
Quite unexpectedly, mice with PPAR-? deficient macrophages were more resistant to
bleomycin-induced weight loss whereas extracellular matrix deposition was
unaffected compared to controls. Therefore PPAR-? expression in macrophages may
be a pathogen-specific limiter of organ recovery rather than a ubiquitous
effector pathway in response to generic damage.
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