Skip Navigation
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

National Institute of Environmental Health Sciences

Use this QR code to view the newest version of this document
Use this QR code to view the newest version of this document

Your Environment. Your Health.

Publication Detail

Title: Nlrp12 mutation causes C57BL/6J strain-specific defect in neutrophil recruitment.

Authors: Ulland, Tyler K; Jain, Nidhi; Hornick, Emma E; Elliott, Eric I; Clay, Gwendolyn M; Sadler, Jeffrey J; Mills, Kathleen A M; Janowski, Ann M; Volk, A Paige Davis; Wang, Kai; Legge, Kevin L; Gakhar, Lokesh; Bourdi, Mohammed; Ferguson, Polly J; Wilson, Mary E; Cassel, Suzanne L; Sutterwala, Fayyaz S

Published In Nat Commun, (2016 10 25)

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.

PubMed ID: 27779193 Exiting the NIEHS site

MeSH Terms: Animals; Base Sequence; Cell Movement; Chemokine CXCL1/deficiency; Chemokine CXCL1/genetics*; Chemokine CXCL1/immunology; Disease Susceptibility; Francisella tularensis/immunology; Gene Expression; Immunity, Innate; Intracellular Signaling Peptides and Proteins/deficiency; Intracellular Signaling Peptides and Proteins/genetics*; Intracellular Signaling Peptides and Proteins/immunology; Lipopolysaccharides/pharmacology; Macrophages/drug effects; Macrophages/immunology; Macrophages/pathology*; Mice; Mice, Inbred C57BL; Mice, Inbred Strains; Mutation*; Neutrophils/drug effects; Neutrophils/immunology; Neutrophils/pathology*; Survival Analysis; Tularemia/genetics; Tularemia/immunology*; Tularemia/microbiology; Tularemia/mortality

Back
to Top