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Redundant roles for inflammasome receptors NLRP3 and NLRC4 in host defense against Salmonella

(2010) JOURNAL OF EXPERIMENTAL MEDICINE. 207(8). p.1745-1755
Author
Organization
Abstract
Intracellular pathogens and endogenous danger signals in the cytosol engage NOD-like receptors (NLRs), which assemble inflammasome complexes to activate caspase-1 and promote the release of proinflammatory cytokines IL-1. and IL-18. However, the NLRs that respond to microbial pathogens in vivo are poorly defined. We show that the NLRs NLRP3 and NLRC4 both activate caspase-1 in response to Salmonella typhimurium. Responding to distinct bacterial triggers, NLRP3 and NLRC4 recruited ASC and caspase-1 into a single cytoplasmic focus, which served as the site of pro-IL-1. processing. Consistent with an important role for both NLRP3 and NLRC4 in innate immune defense against S. typhimurium, mice lacking both NLRs were markedly more susceptible to infection. These results reveal unexpected redundancy among NLRs in host defense against intracellular pathogens in vivo.
Keywords
IPAF, CANDIDA-ALBICANS, DIPEPTIDE, SECRETION, INFECTION, CELL-DEATH, ENTERICA SEROVAR TYPHIMURIUM, PROTEIN, ASC, CASPASE-1 ACTIVATION, MURAMYL DIPEPTIDE

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Citation

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Chicago
Broz, Petr, Kim Newton, Mohamed Lamkanfi, Sanjeev Mariathasan, Vishva M Dixit, and Denise M Monack. 2010. “Redundant Roles for Inflammasome Receptors NLRP3 and NLRC4 in Host Defense Against Salmonella.” Journal of Experimental Medicine 207 (8): 1745–1755.
APA
Broz, P., Newton, K., Lamkanfi, M., Mariathasan, S., Dixit, V. M., & Monack, D. M. (2010). Redundant roles for inflammasome receptors NLRP3 and NLRC4 in host defense against Salmonella. JOURNAL OF EXPERIMENTAL MEDICINE, 207(8), 1745–1755.
Vancouver
1.
Broz P, Newton K, Lamkanfi M, Mariathasan S, Dixit VM, Monack DM. Redundant roles for inflammasome receptors NLRP3 and NLRC4 in host defense against Salmonella. JOURNAL OF EXPERIMENTAL MEDICINE. 2010;207(8):1745–55.
MLA
Broz, Petr, Kim Newton, Mohamed Lamkanfi, et al. “Redundant Roles for Inflammasome Receptors NLRP3 and NLRC4 in Host Defense Against Salmonella.” JOURNAL OF EXPERIMENTAL MEDICINE 207.8 (2010): 1745–1755. Print.
@article{1029452,
  abstract     = {Intracellular pathogens and endogenous danger signals in the cytosol engage NOD-like receptors (NLRs), which assemble inflammasome complexes to activate caspase-1 and promote the release of proinflammatory cytokines IL-1. and IL-18. However, the NLRs that respond to microbial pathogens in vivo are poorly defined. We show that the NLRs NLRP3 and NLRC4 both activate caspase-1 in response to Salmonella typhimurium. Responding to distinct bacterial triggers, NLRP3 and NLRC4 recruited ASC and caspase-1 into a single cytoplasmic focus, which served as the site of pro-IL-1. processing. Consistent with an important role for both NLRP3 and NLRC4 in innate immune defense against S. typhimurium, mice lacking both NLRs were markedly more susceptible to infection. These results reveal unexpected redundancy among NLRs in host defense against intracellular pathogens in vivo.},
  author       = {Broz, Petr and Newton, Kim and Lamkanfi, Mohamed and Mariathasan, Sanjeev and Dixit, Vishva M and Monack, Denise M},
  issn         = {0022-1007},
  journal      = {JOURNAL OF EXPERIMENTAL MEDICINE},
  keyword      = {IPAF,CANDIDA-ALBICANS,DIPEPTIDE,SECRETION,INFECTION,CELL-DEATH,ENTERICA SEROVAR TYPHIMURIUM,PROTEIN,ASC,CASPASE-1 ACTIVATION,MURAMYL DIPEPTIDE},
  language     = {eng},
  number       = {8},
  pages        = {1745--1755},
  title        = {Redundant roles for inflammasome receptors NLRP3 and NLRC4 in host defense against Salmonella},
  url          = {http://dx.doi.org/10.1084/jem.20100257},
  volume       = {207},
  year         = {2010},
}

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