期刊
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
卷 111, 期 1, 页码 385-390出版社
NATL ACAD SCIENCES
DOI: 10.1073/pnas.1317643111
关键词
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资金
- Crohn's and Colitis Foundation of America
- European Research Council [281600]
- Fund for Scientific Research-Flanders [G030212N, 1.2.201.10.N.00, 1.5.122.11.N.00]
- National Institute of Arthritis and Musculoskeletal and Skin Diseases, part of the National Institutes of Health [AR056296]
- National Cancer Institute, part of the National Institutes of Health [CA163507]
- National Institute of Allergy and Infectious Diseases, part of the National Institutes of Health [AI101935]
- American Lebanese Syrian Associated Charities (ALSAC)
The nucleotide-binding oligomerization domain (NOD)-like receptor family pyrin domain containing 12 (NLRP12) plays a protective role in intestinal inflammation and carcinogenesis, but the physiological function of this NLR during microbial infection is largely unexplored. Salmonella enterica serovar Typhimurium (S. typhimurium) is a leading cause of food poisoning worldwide. Here, we show that NLRP12-deficient mice were highly resistant to S. typhimurium infection. Salmonella-infected macrophages induced NLRP12-dependent inhibition of NF-kappa B and ERK activation by suppressing phosphorylation of I kappa B alpha and ERK. NLRP12-mediated down-regulation of proinflammatory and antimicrobial molecules prevented efficient clearance of bacterial burden, highlighting a role for NLRP12 as a negative regulator of innate immune signaling during salmonellosis. These results underscore a signaling pathway defined by NLRP12-mediated dampening of host immune defenses that could be exploited by S. typhimurium to persist and survive in the host.
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