A major role for intestinal epithelial nucleotide oligomerization domain 1 (NOD1) in eliciting host bactericidal immune responses to Campylobacter jejuni

Dorrell, Nick; Elmi, Abdi; Lindley, K. J.; Schüller, Stephanie; Jones, HE; Klein, Nigel; Nuñez, Guillermo Gabriel; Wren, BW; Bajaj-Elliott, Mona

doi:10.1111/j.1462-5822.2007.01008.x

Cited by 29 publications

(26 citation statements)

References 2 publications

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“…The antiinflammatory effects of dietary oleic acid (Vassiliou et al 2009) and n-3-PUFAs (Lee et al 2003) has been suggested to be mediated through the inhibition of TLR-induced signaling pathways, and the possibility that both the beneficial and detrimental effects of different dietary FFA may in part be mediated through the modulation of TLRs (Girardin and Philpott 2004) or NODs (Heim et al 2002). Activation of TLR or NODs synergistically initiates a signaling pathway leading to the activation of NF-B (Tada et al 2005;Zilbauer et al 2007). In fact, activation of TLR and NOD pathways lead to activation of inflammatory pathways.…”

Section: Discussionmentioning

confidence: 99%

PPARγ-dependent peptidoglycan recognition protein 3 (PGlyRP3) expression regulates proinflammatory cytokines by microbial and dietary fatty acids

et al. 2011

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Section: Discussionmentioning

confidence: 99%

PPARγ-dependent peptidoglycan recognition protein 3 (PGlyRP3) expression regulates proinflammatory cytokines by microbial and dietary fatty acids

et al. 2011

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“…Indeed, recent studies demonstrated that RICK is specifically required for NOD1 and NOD2 signaling, but not for TLR pathways . In vitro studies indicated that multiple bacteria including Shigella flexneri (Girardin et al, 2003a), entero-invasive Escherichia coli (Kim et al, 2004), Chlamydophila pneumoniae (Opitz et al, 2005), Campylobacter jejuni (Zilbauer et al, 2007), and Listeria monocytogenes Park et al, 2007) are sensed by NOD1. NOD2 has also been implicated in sensing intracellular pathogens such as Listeria monocytogenes (Kobayashi et al, 2005), Streptococcus pneumoniae (Opitz et al, 2004), and Mycobacterium tuberculosis (Ferwerda et al, 2005).…”

Section: Nlrp9cmentioning

confidence: 99%

Intracellular NOD-like Receptors in Host Defense and Disease

2007

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The innate immune system comprises several classes of pattern recognition receptors, including Toll-like receptors (TLRs), NOD-like receptors (NLRs), and RIG-1-like receptors (RLRs). TLRs recognize microbes on the cell surface and in endosomes, whereas NLRs and RLRs detect microbial components in the cytosol. Here we discuss the recent understanding in NLRs. Two NLRs, NOD1 and NOD2, sense the cytosolic presence of the peptidoglycan fragments meso-DAP and muramyl dipeptide, respectively, and drive the activation of mitogen-activated protein kinase (MAPK) and the transcription factor NF-kappaB. A different set of NLRs induces caspase-1 activation through the assembly of large protein complexes named inflammasomes. Genetic variations in several NLR members are associated with the development of inflammatory disorders. Further understanding of NLRs should provide new insights into the mechanisms of host defense and the pathogenesis of inflammatory diseases.

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“…Specifically, NOD1 recognizes meso-diaminopimelic acid from Gram-negative bacteria and certain Grampositive bacteria [100], whereas NOD2 recognizes muramyl dipeptide (MDP) from Gram-positive and Gram-negative bacteria [101]. These PRRs also recognize various types of pathogenic bacteria; for example, Helicobacter pylori [102], Campylobacter jejuni [103], C. pneumoniae [104] and Enteropathogenic E. coli [105] are sensed by NOD1, whereas NOD2 senses S. pneumoniae [106], M. tuberculosis [107] and S. aureus [108] (Table 1). Activation of NOD1 and NOD2 via PAMP recognition initiates oligomerization of these sensors, leading to recruitment of a CARD-containing adapter protein known as RIP2 (also called RIP-like interacting CLARP kinase [RICK]) by homotypic CARD-CARD interactions.…”

Section: Nod1 and Nod2mentioning

confidence: 99%

Pattern recognition receptors: sentinels in innate immunity and targets of new vaccine adjuvants

Olive

2012

Expert Review of Vaccines

123

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The innate immune system plays an essential role in the host's first line of defense against microbial invasion, and involves the recognition of distinct pathogen-associated molecular patterns by pattern recognition receptors (PRRs). Activation of PRRs triggers cell signaling leading to the production of proinflammatory cytokines, chemokines and Type 1 interferons, and the induction of antimicrobial and inflammatory responses. These innate responses are also responsible for instructing the development of an appropriate pathogen-specific adaptive immune response. In this review, the focus is on different classes of PRRs that have been identified, including Toll-like receptors, nucleotide-binding oligomerization domain-like receptors, and the retinoic acid-inducible gene-I-like receptors, and their importance in host defense against infection. The role of PRR cooperation in generating optimal immune responses required for protective immunity and the potential of targeting PRRs in the development of a new generation of vaccine adjuvants is also discussed.

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A major role for intestinal epithelial nucleotide oligomerization domain 1 (NOD1) in eliciting host bactericidal immune responses to Campylobacter jejuni

Cited by 29 publications

References 2 publications

PPARγ-dependent peptidoglycan recognition protein 3 (PGlyRP3) expression regulates proinflammatory cytokines by microbial and dietary fatty acids

PPARγ-dependent peptidoglycan recognition protein 3 (PGlyRP3) expression regulates proinflammatory cytokines by microbial and dietary fatty acids

Intracellular NOD-like Receptors in Host Defense and Disease

Pattern recognition receptors: sentinels in innate immunity and targets of new vaccine adjuvants

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