Deletion of LysM in LysM-Cre Recombinase Homozygous Mice is Non-Contributory in LPS-Induced Acute Lung Injury
Lysozyme is an important component of the innate immune system, and has roles in peptidoglycan cleavage of gram positive organisms. Myeloid cells highly express the isoform, lysozyme M, and its promoter has been used to direct Cre-recombinase expression to target deletion of floxed genes in myeloid...
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Published in | Lung Vol. 197; no. 6; pp. 819 - 823 |
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Main Authors | , , |
Format | Journal Article |
Language | English |
Published |
08.11.2019
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Online Access | Get full text |
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Summary: | Lysozyme is an important component of the innate immune system, and has
roles in peptidoglycan cleavage of gram positive organisms. Myeloid cells highly
express the isoform, lysozyme M, and its promoter has been used to direct
Cre-recombinase expression to target deletion of floxed genes in myeloid cells.
However, generation of the LysM-Cre mouse effectively disrupts the LysM-gene,
and mice homozygous for the Cre allele lack the LysM gene product. To test the
contribution of LysM in sterile acute lung injury, we generated LysM-Cre mice
homozygous for the Cre allele (+/+) or wild-type allele (−/−).
These mice were challenged with LPS delivered via oropharygneal aspiration. Mice
were monitored and weighed daily, and BAL cell counts, differential, protein,
and cytokine levels were assessed at days 2 and 4. LysMCre+/+ and
LysMCre−/− had similar weight loss and recovery, and similar
inflammatory responses to LPS at days 2 and 4. These findings indicate that that loss
of LysM and expression of Cre-recombinase are non-contributory in sterile acute
lung injury. |
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ISSN: | 0341-2040 1432-1750 |
DOI: | 10.1007/s00408-019-00286-5 |