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

Tyler K. Ulland, Nidhi Jain, Emma E. Hornick, Eric I. Elliott, Gwendolyn M. Clay, Jeffrey J. Sadler, Kathleen A. M. Mills, Ann M. Janowski, A. Paige Davis Volk, Kai Wang, Kevin L. Legge, Lokesh Gakhar, Mohammed Bourdi, Polly J. Ferguson, Mary E. Wilson, Suzanne L. Cassel and Fayyaz S. Sutterwala ()
Additional contact information
Tyler K. Ulland: Inflammation Program, University of Iowa Carver College of Medicine
Nidhi Jain: Inflammation Program, University of Iowa Carver College of Medicine
Emma E. Hornick: Inflammation Program, University of Iowa Carver College of Medicine
Eric I. Elliott: Inflammation Program, University of Iowa Carver College of Medicine
Gwendolyn M. Clay: Interdisciplinary Program in Molecular and Cellular Biology, University of Iowa Carver College of Medicine
Jeffrey J. Sadler: Inflammation Program, University of Iowa Carver College of Medicine
Kathleen A. M. Mills: Inflammation Program, University of Iowa Carver College of Medicine
Ann M. Janowski: Inflammation Program, University of Iowa Carver College of Medicine
A. Paige Davis Volk: Inflammation Program, University of Iowa Carver College of Medicine
Kai Wang: University of Iowa College of Public Health
Kevin L. Legge: Interdisciplinary Program in Immunology, University of Iowa Carver College of Medicine
Lokesh Gakhar: University of Iowa Carver College of Medicine
Mohammed Bourdi: Molecular and Cellular Toxicology Section, Laboratory of Molecular Immunology, National Heart, Lung and Blood Institute, National Institutes of Health
Polly J. Ferguson: University of Iowa Carver College of Medicine
Mary E. Wilson: Interdisciplinary Program in Molecular and Cellular Biology, University of Iowa Carver College of Medicine
Suzanne L. Cassel: Inflammation Program, University of Iowa Carver College of Medicine
Fayyaz S. Sutterwala: Inflammation Program, University of Iowa Carver College of Medicine

Nature Communications, 2016, vol. 7, issue 1, 1-13

Abstract: 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.

Date: 2016
References: Add references at CitEc
Citations:

Downloads: (external link)
https://www.nature.com/articles/ncomms13180 Abstract (text/html)

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:7:y:2016:i:1:d:10.1038_ncomms13180

Ordering information: This journal article can be ordered from
https://www.nature.com/ncomms/

DOI: 10.1038/ncomms13180

Access Statistics for this article

Nature Communications is currently edited by Nathalie Le Bot, Enda Bergin and Fiona Gillespie

More articles in Nature Communications from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().