Salmonella exploits NLRP12-dependent innate immune signaling to suppress host defenses during infection

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...

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Published in	Proceedings of the National Academy of Sciences - PNAS Vol. 111; no. 1; pp. 385 - 390
Main Authors	Zaki, Md. Hasan, Man, Si Ming, Vogel, Peter, Lamkanfi, Mohamed, Kanneganti, Thirumala-Devi
Format	Journal Article
Language	English
Published	United States National Academy of Sciences 07.01.2014 National Acad Sciences
Subjects	Animals Bacterial infections Biological Sciences Bone Marrow Cells - immunology Bone Marrow Cells - microbiology Cytokines Digestive system Extracellular Signal-Regulated MAP Kinases - metabolism Food contamination & poisoning Host-Pathogen Interactions Immunity (Disease) Immunity, Innate Infections Inflammation Intracellular Signaling Peptides and Proteins - metabolism Liver Liver - metabolism Macrophages Macrophages - microbiology Male Mice Mice, Transgenic Models, Biological Molecules NF-kappa B - metabolism Nitric Oxide - chemistry Nucleotides - chemistry Pathogens Phosphorylation Protein Structure, Tertiary Receptors Salmonella Salmonella enterica Salmonella infections Salmonella Infections, Animal - immunology Salmonella Infections, Animal - microbiology Salmonella typhimurium Salmonella typhimurium - metabolism Signal Transduction Time Factors
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Abstract	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-κB and ERK activation by suppressing phosphorylation of IκBα 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.
AbstractList	Salmonella enterica serovar Typhimurium ( S. typhimurium ) is a bacterial foodborne pathogen that causes significant morbidity and mortality worldwide. Nucleotide-binding oligomerization domain–like receptor family pyrin domain containing 12 NLRP12 is a key innate immune molecule that regulates intestinal inflammation and cancer. However, its physiological function in microbial infection is not fully understood. We found that NLRP12 is a key suppressor of innate immune signaling during salmonellosis. Mice lacking NLRP12 are hyperresistant to S. typhimurium infection, and macrophages deficient in NLRP12 produce high levels of proinflammatory cytokines and other molecules contributing to pathogen clearance. Our work revealed that NLRP12-mediated dampening of host immune defenses is used by S. typhimurium to ensure its persistence and survival in host tissues. Modulation of NLRP12 activity could be useful in the prevention and treatment of salmonellosis. 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-κB and ERK activation by suppressing phosphorylation of IκBα 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. 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-...B and ERK activation by suppressing phosphorylation of I...B... 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. (ProQuest: ... denotes formulae/symbols omitted.) 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-κB and ERK activation by suppressing phosphorylation of IκBα 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. 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-B and ERK activation by suppressing phosphorylation of IB 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. Significance Salmonella enterica serovar Typhimurium ( S. typhimurium ) is a bacterial foodborne pathogen that causes significant morbidity and mortality worldwide. Nucleotide-binding oligomerization domain–like receptor family pyrin domain containing 12 NLRP12 is a key innate immune molecule that regulates intestinal inflammation and cancer. However, its physiological function in microbial infection is not fully understood. We found that NLRP12 is a key suppressor of innate immune signaling during salmonellosis. Mice lacking NLRP12 are hyperresistant to S. typhimurium infection, and macrophages deficient in NLRP12 produce high levels of proinflammatory cytokines and other molecules contributing to pathogen clearance. Our work revealed that NLRP12-mediated dampening of host immune defenses is used by S. typhimurium to ensure its persistence and survival in host tissues. Modulation of NLRP12 activity could be useful in the prevention and treatment of salmonellosis. 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-κB and ERK activation by suppressing phosphorylation of IκBα 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.
Author	Kanneganti, Thirumala-Devi Vogel, Peter Zaki, Md. Hasan Man, Si Ming Lamkanfi, Mohamed
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Notes	http://dx.doi.org/10.1073/pnas.1317643111 ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Author contributions: M.H.Z. and T.-D.K. designed research; M.H.Z., S.M.M., and P.V. performed research; M.H.Z., S.M.M., P.V., M.L., and T.-D.K. analyzed data; and M.H.Z., S.M.M., M.L., and T.-D.K. wrote the paper. 1Present address: Department of Pathology, University of Texas Southwestern Medical Center, Dallas, TX 75390. Edited by Vishva M. Dixit, Genentech, San Francisco, CA, and approved November 20, 2013 (received for review September 18, 2013)
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Snippet	The nucleotide-binding oligomerization domain (NOD)-like receptor family pyrin domain containing 12 (NLRP12) plays a protective role in intestinal inflammation... Significance Salmonella enterica serovar Typhimurium ( S. typhimurium ) is a bacterial foodborne pathogen that causes significant morbidity and mortality... Salmonella enterica serovar Typhimurium ( S. typhimurium ) is a bacterial foodborne pathogen that causes significant morbidity and mortality worldwide....
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SubjectTerms	Animals Bacterial infections Biological Sciences Bone Marrow Cells - immunology Bone Marrow Cells - microbiology Cytokines Digestive system Extracellular Signal-Regulated MAP Kinases - metabolism Food contamination & poisoning Host-Pathogen Interactions Immunity (Disease) Immunity, Innate Infections Inflammation Intracellular Signaling Peptides and Proteins - metabolism Liver Liver - metabolism Macrophages Macrophages - microbiology Male Mice Mice, Transgenic Models, Biological Molecules NF-kappa B - metabolism Nitric Oxide - chemistry Nucleotides - chemistry Pathogens Phosphorylation Protein Structure, Tertiary Receptors Salmonella Salmonella enterica Salmonella infections Salmonella Infections, Animal - immunology Salmonella Infections, Animal - microbiology Salmonella typhimurium Salmonella typhimurium - metabolism Signal Transduction Time Factors
Title	Salmonella exploits NLRP12-dependent innate immune signaling to suppress host defenses during infection
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