NOD-like receptors and the innate immune system: Coping with danger, damage and death

Kersse, Kristof; Bertrand, Mathieu J.M.; Lamkanfi, Mohamed; Vandenabeele, Peter

doi:10.1016/j.cytogfr.2011.09.003

Cited by 175 publications

(154 citation statements)

References 346 publications

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“…The family of NOD-like receptors (NLRs) includes 23 members in humans and 34 in mice [31,69]. These cytoplasmic receptors contain a leucine-rich repeats (LRR) domain, which senses bacterial ligands, a central NOD domain (also called NATCH domain) required for activation and an N-terminal effector domain that mediates interactions with other signaling proteins.…”

Section: Immune Dysregulationmentioning

confidence: 99%

“…As described in the next section, PRRs play an essential role in the host microbial interaction by sensing conserved microbial structures (pathogen-associated molecular patterns, PAMPs). Binding of PAMPs results in the activation of multiple signaling pathways including nuclear factor-B (NF-B) and mitogen activated protein kinases (MAPKs), which in turn induce the production of inflammatory mediators and also initiate multiple cellular processes, including cell proliferation and differentiation [30][31][32]. NOD2, a member of the nucleotide-binding oligomerization domain (NOD)-like receptor (NLR) family, recognizes muramyl dipeptide (MDP), a component of peptidoglycan (PGN) in nearly all bacteria [30].…”

Section: Pathomechanism 21 Genetic Susceptibilitymentioning

confidence: 99%

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Gut Inflammation: Current Update on Pathophysiology, Molecular Mechanism and Pharmacological Treatment Modalities

Gyires¹,

Tóth²,

Zádori

2014

CPD

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Inflammatory bowel disease (IBD) is a chronic and relapsing inflammatory condition of the gastrointestinal tract. The two main forms of IBD are Crohn's disease and ulcerative colitis. According to the recent concept the disease is caused by a combination of factors, including genetics, immune dysregulation, barrier dysfunction and the change in microbial flora. Environmental factors, such as changes in diet, antibiotic use, smoking or improved domestic hygiene (e.g. eradication of intestinal helminths) probably contribute to the development and increased prevalence of IBD. Dysregulation of mucosal immunity in IBD causes an overproduction of inflammatory cytokines which resulted in uncontrolled intestinal inflammation. Based on extensive research over the last decade, besides the conventional therapy, there are several novel pathways and specific targets, on which focus new therapeutics. New therapeutics aim 1./ to correct genetic susceptibility by stimulating NOD2 expression, TLR3 signaling or inhibition of TLR4 pathway, 2./ to restore the immune dysregulation by inhibition of pro-inflammatory cytokines (TNF-, IL-6, IL-13, IL-17, IL-18, IL-21), Th1 polarisation (IL-2, IL-12, IL-23, IFN-), T-cell activation, leukocyte adhesion, as well as by immunostimulation (GM-CSF, G-CSF) and anti-inflammatory cytokines (IL-10, IL-11, IFN--1a), 3./ to restore mucosal barrier function and stimulate mucosal healing by different growth factors, such as GH, EGF, KGF, TGF-, VEGF, 4./ to restore the normal bacterial flora by antibiotics, probiotics. However, in spite of these numerous potential targets, the true value and clinical significance of most of the new biologics and molecules are not clear yet.

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Section: Immune Dysregulationmentioning

confidence: 99%

Section: Pathomechanism 21 Genetic Susceptibilitymentioning

confidence: 99%

Gut Inflammation: Current Update on Pathophysiology, Molecular Mechanism and Pharmacological Treatment Modalities

Gyires¹,

Tóth²,

Zádori

2014

CPD

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“…The main pattern recognition receptors involved in initial pneumococcus sensing in the CNS are Tolllike 2 receptors (TRL-2 or CD282) that is recognized by peptidoglycans and lipoteichoic acids 17 , Toll-like 4 receptors (TRL-4 or CD284) that are recognized by exotoxin pneumolysin 18 and the Toll-Like 9 receptors (TRL-9 or CD289), an intracellular pattern recognition receptor that is activated by CpG in bacterial DNA 19 . Family members of the NOD-like receptors (NLRs), which are intracellular, play essential roles on innate immunity by detecting intracellular pathogen-associated molecular patterns 20 . When they are activated, they induce the activation of nuclear factor kappa B (NF-κB) or mitogen-activated protein kinase (MAPK) pathways and inflammatory caspases 21 .…”

Section: Central Nervous System Bacterial Invasionmentioning

confidence: 99%

Pathophysiology of acute meningitis caused by Streptococcus pneumoniae and adjunctive therapy approaches

Barichello

Generoso

Collodel

et al. 2012

Arq. Neuro-Psiquiatr.

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Pneumococcal meningitis is a life-threatening disease characterized by an acute purulent infection affecting piamater, arachnoid and the subarachnoid space. The intense inflammatory host's response is potentially fatal and contributes to the neurological sequelae. Streptococcus pneumoniae colonizes the nasopharynx, followed by bacteremia, microbial invasion and blood-brain barrier traversal. S. pneumoniae is recognized by antigen-presenting cells through the binding of Toll-like receptors inducing the activation of factor nuclear kappa B or mitogen-activated protein kinase pathways and subsequent up-regulation of lymphocyte populations and expression of numerous proteins involved in inflammation and immune response. Many brain cells can produce cytokines, chemokines and others pro-inflammatory molecules in response to bacteria stimuli, as consequence, polymorphonuclear are attracted, activated and released in large amounts of superoxide anion and nitric oxide, leading to the peroxynitrite formation, generating oxidative stress. This cascade leads to lipid peroxidation, mitochondrial damage, blood-brain barrier breakdown contributing to cell injury during pneumococcal meningitis.

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“…This complex supports the autocatalytic cleavage of caspase-1 which enables the processing and secretion of IL-1 and IL-18. NLRP1, NLRP3, NLRC4 and the adapter apoptosis-associated speck-like protein containing a CARD (ASC) are critical components of the inflammasome but emerging components include NLRP6 (Bauernfeind 2011, Ablasser et al;Kersse 2011, Bertrand et al;Franchi, Eigenbrod et al 2009). While much of the focus has been on the caspase-1 inflammasome, other caspases are also associated with an inflammasome-triggered response in a caspase-1-independent manner (Kayagaki, Warming et al 2011).…”

Section: The Inflammasomementioning

confidence: 99%

Cytokines and the Innate Immune Response at the Materno-Fetal Interface

Bryant¹,

Thornton²

2012

Recent Advances in Research on the Human Placenta

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NOD-like receptors and the innate immune system: Coping with danger, damage and death

Cited by 175 publications

References 346 publications

Gut Inflammation: Current Update on Pathophysiology, Molecular Mechanism and Pharmacological Treatment Modalities

Gut Inflammation: Current Update on Pathophysiology, Molecular Mechanism and Pharmacological Treatment Modalities

Pathophysiology of acute meningitis caused by Streptococcus pneumoniae and adjunctive therapy approaches

Cytokines and the Innate Immune Response at the Materno-Fetal Interface

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