Nod1, Nod2 and Nalp3 receptors, new potential targets in treatment of allergic rhinitis?

Bogefors, Jesper; Rydberg, Camilla; Uddman, Rolf; Fransson, Mattias; Månsson, Alf; Benson, Mikael; Adner, Mikael; Cardell, Lars-Olaf

doi:10.1111/j.1398-9995.2009.02315.x

Cited by 47 publications

(50 citation statements)

References 17 publications

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“…NLRP3 has been shown to sense asbestos and uric acid as a result of lung injury (180)(181)(182). NLRP3 is present in the nasal epithelium, and in vivo NLRP3 null mice show reduced inflammation to bacterial and viral challenge but poor survival, showcasing the requirement for inflammation in clearing infections (151,165,166,183).…”

Section: Bacterial Activation Of the Inflammasomementioning

confidence: 99%

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Innate Immunity in the Respiratory Epithelium

Parker

Prince

2011

Am J Respir Cell Mol Biol

386

404

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The airway epithelium represents the first point of contact for inhaled foreign organisms. The protective arsenal of the airway epithelium is provided in the form of physical barriers and a vast array of receptors and antimicrobial compounds that constitute the innate immune system. Many of the known innate immune receptors, including the Toll-like receptors and nucleotide oligomerization domain-like receptors, are expressed by the airway epithelium, which leads to the production of proinflammatory cytokines and chemokines that affect microorganisms directly and recruit immune cells, such as neutrophils and T cells, to the site of infection. The airway epithelium also produces a number of resident antimicrobial proteins, such as lysozyme, lactoferrin, and mucins, as well as a swathe of cationic proteins. Dysregulation of the airway epithelial innate immune system is associated with a number of medical conditions that can result in compromised immunity and chronic inflammation of the lung. This review focuses on the innate immune capabilities of the airway epithelium and its role in protecting the lung from infection as well as the outcomes when its function is compromised.

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Section: Bacterial Activation Of the Inflammasomementioning

confidence: 99%

“…Both NOD proteins are expressed in the airway epithelium and are induced with bacterial stimuli (30,(151)(152)(153)(154). In the context of polymicrobial colonization in the airway, the pore-forming toxin pneumolysin from S. pneumoniae facilitates entry of peptidoglycan from Haemophilus influenzae to activate NOD1 (155).…”

Section: Nod-like Receptorsmentioning

confidence: 99%

Innate Immunity in the Respiratory Epithelium

Parker

Prince

2011

Am J Respir Cell Mol Biol

386

404

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“…In humans, genome-wide association studies have revealed a molecular link between polymorphisms of NOD1, asthma, and high levels of serum IgE (10) as well as with atopic dermatitis (11) and allergic rhinitis (12). NOD1 gene expression changes have been found in nasal mucosa from patients with rhinitis during the pollen season (13). However, the functionality of NOD1 in human allergic asthma remains elusive.…”

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confidence: 99%

CCL17 Production by Dendritic Cells Is Required for NOD1-mediated Exacerbation of Allergic Asthma

Yahia

Azzaoui

Everaere

et al. 2014

Am J Respir Crit Care Med

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“…Both NOD1 and NOD2 are highly expressed in immune and inflammatory cells (Fritz et al, 2005;Kanneganti et al, 2007). These two NODs are also expressed in airway epithelium and are induced by bacterial stimuli (Bogefors et al, 2010;Mayer et al, 2007;Opitz et al, 2004;Travassos et al, 2005). NOD1 and NOD2 contribute to innate immune responses to different bacteria including Pseudomonas aeruginosa, Chlamydia pneumonia, Haemophilus influenza and L. pneumophila both in vivo and in vitro (Clarke et al, 2010;Frutuoso et al, 2010;Shimada et al, 2009;Zola et al, 2008).…”

Section: Nod-like Receptorsmentioning

confidence: 99%