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Hepatocyte-specific S100a8 and S100a9 transgene expression in mice causes Cxcl1 induction and systemic neutrophil enrichment
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Hepatocyte-specific S100a8 and S100a9 transgene expression in mice causes Cxcl1 induction and systemic neutrophil enrichment
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Hepatocyte-specific S100a8 and S100a9 transgene expression in mice causes Cxcl1 induction and systemic neutrophil enrichment
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Journal Article
Hepatocyte-specific S100a8 and S100a9 transgene expression in mice causes Cxcl1 induction and systemic neutrophil enrichment
2012
Overview
Background
Calprotectin consists of the Ca
2+
-binding proteins S100a8 and S100a9 that are induced in epithelial cells in response to tissue damage and infection. Both proteins are also secreted by activated innate immune cells and numerous studies demonstrate their crucial role in pathological conditions of acute and chronic inflammation.
Results
Here, we established a conditional mouse model with simultaneous
S100a8
and
S100a9
transgene expression in hepatocytes (
TgS100a8a9
hep
) under the control of doxycycline to unravel the role of epithelial-derived Calprotectin on tissue homeostasis and inflammation.
TgS100a8a9
hep
mice displayed a significant enrichment of neutrophils in peripheral blood and tissues with high blood content. Interestingly,
Cxcl1
transcription was significantly induced in the liver of
TgS100a8a9
hep
mice and primary hepatocytes derived thereof as compared to Control mice, accompanied by an increase of Cxcl1 serum levels. However, expression of other chemokines with a known function in neutrophil mobilization from the bone marrow, e.g. Csf3 and Cxcl2, was not altered. Doxycycline treatment of
TgS100a8a9
hep
mice reduced
Cxcl1
expression in the liver and resulted in normal numbers of neutrophils.
Conclusion
In summary, our data demonstrate for the first time that hepatocyte-specific S100a8 and S100a9 expression induces a systemic mobilization of neutrophils by a specific activation of Cxcl1 transcription in the liver.
Publisher
BioMed Central,BioMed Central Ltd,Springer Nature B.V,BMC
Subject
