ArticleLung2019
Deletion of LysM in LysMCre Recombinase Homozygous Mice is Non-contributory in LPS-Induced Acute Lung Injury.
Article in Lung, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 14 citations in OpenAlex.
- Assessment of Noninvasive Measurement Techniques and Histologic Findings in a Mouse Model of LPS-Induced Acute Lung Injury.Journal of the American Association for Laboratory Animal Science : JAALAS · 2026Article
- Myeloid monoamine oxidase A protects against glucose intolerance, insulin resistance and weight gain in high-fat diet-fed mice by preventing the hyperactivation of macrophages.The Journal of nutritional biochemistry · 2026Article
- Proinflammatory keratinocytes drive a novel mouse model of autoimmunity with systemic and cutaneous lupus erythematosus.Immunity & inflammation · 2026Article
- Comprehensive analysis of myeloid reporter mice.bioRxiv : the preprint server for biology · 2025Article
- Mitochondria complex III-generated superoxide is essential for IL-10 secretion in macrophages.Science advances · 2025Article
- Myeloid PDLIM2 repression as a common mechanism of infection susceptibility in lung diseases.Frontiers in immunology · 2025Article
- Metabolic phenotypes in a Lyz2Cre recombinase mouse model.Frontiers in immunology · 2025Article
- IRF3 inhibits inflammatory signaling pathways in macrophages to prevent viral pathogenesis.Science advances · 2024Article
- Mineralocorticoid receptor promotes cardiac macrophage inflammaging.Basic research in cardiology · 2024Article
- Neutrophil-specific STAT4 deficiency attenuates atherosclerotic burden and improves plaque stability via reduction in neutrophil activation and recruitment into aortas ofbioRxiv : the preprint server for biology · 2023Article
- Neutrophil-specific STAT4 deficiency attenuates atherosclerotic burden and improves plaque stability via reduction in neutrophil activation and recruitment into aortas ofFrontiers in cardiovascular medicine · 2023Article
- The complement receptor C5aR2 regulates neutrophil activation and function contributing to neutrophil-driven epidermolysis bullosa acquisita.Frontiers in immunology · 2023Article
- Angiotensin II enhances bacterial clearance via myeloid signaling in a murine sepsis model.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- The role of TBK1 in cancer pathogenesis and anticancer immunity.Journal of experimental & clinical cancer research : CR · 2022Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
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 LysMCre 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 LysMCre 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 loss of LysM and expression of Cre recombinase are non-contributory in sterile acute lung injury.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.