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; Fayyaz S. Sutterwala

doi:10.1038/ncomms13180

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, Fayyaz S. Sutterwala

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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.

Original language	English (US)
Article number	13180
Journal	Nature communications
Volume	7
DOIs	https://doi.org/10.1038/ncomms13180
State	Published - Oct 25 2016

ASJC Scopus subject areas

General Physics and Astronomy
General Chemistry
General Biochemistry, Genetics and Molecular Biology

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Ulland, T. K., Jain, N., Hornick, E. E., Elliott, E. I., Clay, G. M., Sadler, J. J., Mills, K. A. M., Janowski, A. M., Volk, A. P. D., Wang, K., Legge, K. L., Gakhar, L., Bourdi, M., Ferguson, P. J., Wilson, M. E., Cassel, S. L., & Sutterwala, F. S. (2016). Nlrp12 mutation causes C57BL/6J strain-specific defect in neutrophil recruitment. Nature communications, 7, Article 13180. https://doi.org/10.1038/ncomms13180

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title = "Nlrp12 mutation causes C57BL/6J strain-specific defect in neutrophil recruitment",

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.",

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

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doi = "10.1038/ncomms13180",

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AU - Jain, Nidhi

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AU - Clay, Gwendolyn M.

AU - Sadler, Jeffrey J.

AU - Mills, Kathleen A.M.

AU - Janowski, Ann M.

AU - Volk, A. Paige Davis

AU - Wang, Kai

AU - Legge, Kevin L.

AU - Gakhar, Lokesh

AU - Bourdi, Mohammed

AU - Ferguson, Polly J.

AU - Wilson, Mary E.

AU - Cassel, Suzanne L.

AU - Sutterwala, Fayyaz S.

PY - 2016/10/25

Y1 - 2016/10/25

N2 - 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.

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

Abstract

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