dc.contributor.author
Dietert, Kristina
dc.contributor.author
Reppe, Katrin
dc.contributor.author
Mundhenk, Lars
dc.contributor.author
Witzenrath, Martin
dc.contributor.author
Gruber, Achim D.
dc.date.accessioned
2018-06-08T03:55:35Z
dc.date.available
2015-02-17T12:34:59.253Z
dc.identifier.uri
https://refubium.fu-berlin.de/handle/fub188/16226
dc.identifier.uri
http://dx.doi.org/10.17169/refubium-20410
dc.description.abstract
The human hCLCA1 and its murine ortholog mCLCA3 (calcium-activated chloride
channel regulators) are exclusively expressed in mucus cells and linked to
inflammatory airway diseases with increased mucus production, such as asthma,
cystic fibrosis and chronic obstructive pulmonary disease. Both proteins have
a known impact on the mucus cell metaplasia trait in these diseases. However,
growing evidence points towards an additional role in innate immune responses.
In the current study, we analyzed Staphylococcus aureus pneumonia, an
established model to study pulmonary innate immunity, in mCLCA3-deficient and
wild-type mice, focusing on the cellular and cytokine-driven innate
inflammatory response. We compared clinical signs, bacterial clearance,
leukocyte immigration and cytokine responses in the bronchoalveolar
compartment, as well as pulmonary vascular permeability, histopathology, mucus
cell number and mRNA expression levels of selected genes (mClca1 to 7, Muc5ac,
Muc5b, Muc2, Cxcl-1, Cxcl-2, Il-17). Deficiency of mCLCA3 resulted in
decreased neutrophilic infiltration into the bronchoalveolar space during
bacterial infection. Only the cytokines IL-17 and the murine CXCL-8 homolog
CXCL-1 were decreased on mRNA and protein levels during bacterial infection in
mCLCA3-deficient mice compared to wild-type controls. However, no differences
in clinical outcome, histopathology or mucus cell metaplasia were observed. We
did not find evidence for regulation of any other CLCA homolog that would
putatively compensate for the lack of mCLCA3. In conclusion, mCLCA3 appears to
modulate leukocyte response via IL-17 and murine CXCL-8 homologs in acute
Staphylococcus aureus pneumonia which is well in line with the proposed
function of hCLCA1 as a signaling molecule acting on alveolar macrophages.
de
dc.rights.uri
http://creativecommons.org/licenses/by/4.0/
dc.subject.ddc
600 Technik, Medizin, angewandte Wissenschaften::630 Landwirtschaft
dc.title
mCLCA3 Modulates IL-17 and CXCL-1 Induction and Leukocyte Recruitment in
Murine Staphylococcus aureus Pneumonia
dc.type
Wissenschaftlicher Artikel
dcterms.bibliographicCitation
PLoS ONE. - 9 (2014), 7, Artikel Nr. e102606
dcterms.bibliographicCitation.doi
10.1371/journal.pone.0102606
dcterms.bibliographicCitation.url
http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0102606
refubium.affiliation
Veterinärmedizin
de
refubium.mycore.fudocsId
FUDOCS_document_000000020757
refubium.note.author
Der Artikel wurde in einer Open-Access-Zeitschrift publiziert.
refubium.resourceType.isindependentpub
no
refubium.mycore.derivateId
FUDOCS_derivate_000000003788
dcterms.accessRights.openaire
open access