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@ARTICLE{Bhattacharya:274178,
author = {S. Bhattacharya and A. J. Maupin and A. G. Schlosser and
E.-M. Füchtbauer and Y. C. Gloria and A. Weber$^*$ and U.
Holmskov and J. B. Moeller and S. P. Templeton},
title = {{T}he role of {FIBCD}1 in response to {A}spergillus
fumigatus in lung epithelial cells.},
journal = {PLOS ONE},
volume = {18},
number = {3},
issn = {1932-6203},
address = {San Francisco, California, US},
publisher = {PLOS},
reportid = {DKFZ-2023-00473},
pages = {e0282347 -},
year = {2023},
abstract = {Chitin, a polysaccharide, is ubiquitously found in nature
and has been known to be an active immunogen in mammals, and
interacts with Toll-like, mannose and glucan receptors, to
induce cytokine and chemokine secretions. FIBCD1 is a
tetrameric type II transmembrane endocytic vertebrate
receptor that binds chitin, is found in human lung
epithelium and modulates lung epithelial inflammatory
responses to A. fumigatus cell wall polysaccharides. We
previously reported the detrimental role of FIBCD1 in a
murine model of pulmonary invasive aspergillosis. However,
the effect that chitin and chitin-containing A. fumigatus
conidia exerts on lung epithelium following exposure through
FIBCD1 is not yet fully explored. Using both in vitro and in
vivo strategies, we examined how lung and lung epithelial
gene expression are modified after exposure to fungal
conidia or chitin fragments in the presence or absence of
FIBCD1. FIBCD1 expression was associated with a decrease in
inflammatory cytokines with increasing size of chitin
(dimer-oligomer). Thus, our results demonstrate that FIBCD1
expression modulates cytokine and chemokine expression in
response to A. fumigatus conidia that is modified by the
presence of chitin particles.},
cin = {TU01},
ddc = {610},
cid = {I:(DE-He78)TU01-20160331},
pnm = {899 - ohne Topic (POF4-899)},
pid = {G:(DE-HGF)POF4-899},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:36888604},
doi = {10.1371/journal.pone.0282347},
url = {https://inrepo02.dkfz.de/record/274178},
}