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@ARTICLE{Zhang:163745,
author = {Zhang, Jin and Li, Zhenghui and Chandrasekar, Akila and Li,
Shun and Ludolph, Albert and Böckers, Tobias and
Huber-Lang, Markus and Roselli, Francesco and Olde Heuvel,
Florian},
title = {{F}ast {M}aturation of {S}plenic {D}endritic {C}ells {U}pon
{TBI} {I}s {A}ssociated {W}ith {FLT}3/{FLT}3{L}
{S}ignaling.},
journal = {Frontiers in immunology},
volume = {13},
issn = {1664-3224},
address = {Lausanne},
publisher = {Frontiers Media},
reportid = {DZNE-2022-00484},
pages = {824459},
year = {2022},
abstract = {The consequences of systemic inflammation are a significant
burden after traumatic brain injury (TBI), with almost all
organs affected. This response consists of inflammation and
concurrent immunosuppression after injury. One of the main
immune regulatory organs, the spleen, is highly interactive
with the brain. Along this brain-spleen axis, both nerve
fibers as well as brain-derived circulating mediators have
been shown to interact directly with splenic immune cells.
One of the most significant comorbidities in TBI is acute
ethanol intoxication (EI), with almost $40\%$ of patients
showing a positive blood alcohol level (BAL) upon injury. EI
by itself has been shown to reduce proinflammatory mediators
dose-dependently and enhance anti-inflammatory mediators in
the spleen. However, how the splenic immune modulatory
effect reacts to EI in TBI remains unclear. Therefore, we
investigated early splenic immune responses after TBI with
and without EI, using gene expression screening of cytokines
and chemokines and fluorescence staining of thin spleen
sections to investigate cellular mechanisms in immune cells.
We found a strong FLT3/FLT3L induction 3 h after TBI, which
was enhanced by EI. The FLT3L induction resulted in
phosphorylation of FLT3 in CD11c+ dendritic cells, which
enhanced protein synthesis, maturation process, and the
immunity of dendritic cells, shown by pS6, peIF2A, MHC-II,
LAMP1, and CD68 by immunostaining and TNF-α expression by
in-situ hybridization. In conclusion, these data indicate
that TBI induces a fast maturation and immunity of dendritic
cells which is associated with FLT3/FLT3L signaling and
which is enhanced by EI prior to TBI.},
keywords = {Brain Injuries, Traumatic: metabolism / Dendritic Cells /
Humans / Inflammation / Membrane Proteins: genetics / Spleen
/ fms-Like Tyrosine Kinase 3 / FLT3 (Other) / dendritic cell
(Other) / ethanol (Other) / spleen (Other) / traumatic brain
injury (Other)},
cin = {Clinical Study Center Ulm / AG Böckers / AG Roselli},
ddc = {610},
cid = {I:(DE-2719)5000077 / I:(DE-2719)1910002 /
I:(DE-2719)1910001},
pnm = {353 - Clinical and Health Care Research (POF4-353) / 352 -
Disease Mechanisms (POF4-352)},
pid = {G:(DE-HGF)POF4-353 / G:(DE-HGF)POF4-352},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:35281004},
pmc = {pmc:PMC8907149},
doi = {10.3389/fimmu.2022.824459},
url = {https://pub.dzne.de/record/163745},
}