Nlrp12 mutation causes C57BL/6J strain-specific defect in neutrophil recruitment.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 27779193.
- Also identified by DOI 10.1038/ncomms13180 and PMC identifier 5093323.
- Licence recorded as CC BY.
- The licence permits redistribution, so the abstract is shown in full and the full text is available from the publisher.
Abstract
The inbred mouse strain C57BL/6J is widely used in models of immunological and infectious diseases. Here we show that C57BL/6J mice have a defect in neutrophil recruitment to a range of inflammatory stimuli compared with the related C57BL/6N substrain. This immune perturbation is associated with a missense mutation in Nlrp12 in C57BL/6J mice. Both C57BL/6J and NLRP12-deficient mice have increased susceptibility to bacterial infection that correlates with defective neutrophil migration. C57BL/6J and NLRP12-deficient macrophages have impaired CXCL1 production and the neutrophil defect observed in C57BL/6J and NLRP12-deficient mice is rescued by restoration of macrophage NLRP12. These results demonstrate that C57BL/6J mice have a functional defect in NLRP12 and that macrophages require NLRP12 expression for effective recruitment of neutrophils to inflammatory sites.
Medical subject headings
- Chemokine CXCL1
- Intracellular Signaling Peptides and Proteins
- Macrophages
- Mutation
- Neutrophils
- Tularemia