NOD-like receptors in the human upper airways: a potential role in nasal polyposis

Månsson, Alf; Bogefors, Jesper; Cervin, Anders; Uddman, Rolf; Cardell, Lars-Olaf

doi:10.1111/j.1398-9995.2010.02527.x

Cited by 39 publications

(44 citation statements)

References 35 publications

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“…Relevant to our finding of NRLP3 in the normal mouse bronchiolar epithelium is the recent observation reporting NRLP3 and two other NLRs (NOD1 and NOD2) in upper airway human tissues including normal nasal mucosa, nasal polyps, tonsils, and adenoids [29]. It is likely therefore that inflammasome components are present along the entire length of the airways and constitute a front-line defence.…”

Section: Discussionsupporting

confidence: 66%

Immunolocalization of NLRP3 Inflammasome in Normal Murine Airway Epithelium and Changes following Induction of Ovalbumin-Induced Airway Inflammation

et al. 2012

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Little is known about innate immunity and components of inflammasomes in airway epithelium. This study evaluated immunohistological evidence for NLRP3 inflammasomes in normal and inflamed murine (Balb/c) airway epithelium in a model of ovalbumin (OVA) induced allergic airway inflammation. The airway epithelium of control mice exhibited strong cytoplasmic staining for total caspase-1, ASC, and NLRP3, whereas the OVA mice exhibited strong staining for active caspase-1, with redistribution of caspase-1, IL-1β and IL-18, indicating possible activation of the NLRP3 inflammasome. Active caspase-1, NLRP3, and other inflammasome components were also detected in tissue eosinophils from OVA mice, and may potentially contribute to IL-1β and IL-18 production. In whole lung, inRNA expression of NAIP and procaspase-1 was increased in OVA mice, whereas NLRP3, IL-1β and IL-18 decreased. Some OVA-treated mice also had significantly elevated and tightly correlated serum levels of IL-1β and TNFα. In cultured normal human bronchial epithelial cells, LPS priming resulted in a significant increase in NLRP3 and II-lp protein expression. This study is the first to demonstrate NLRP3 inflammasome components in normal airway epithelium and changes with inflammation. We propose activation and/or luminal release of the inflammasome is a feature of allergic airway inflammation which may contribute to disease pathogenesis.

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Section: Discussionsupporting

confidence: 66%

Immunolocalization of NLRP3 Inflammasome in Normal Murine Airway Epithelium and Changes following Induction of Ovalbumin-Induced Airway Inflammation

et al. 2012

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“…It has previously been reported that high NLRP3 mRNA levels were detected in neutrophils, macrophages [2], and primary immune cells [14], while NLRP3 protein was only detected in lymphoid tissues by western blot, and not by IHC, using an in-house generated monoclonal antibody. In 2011, Månsson et al [16] reported that NALP3 mRNA and protein were present in nasal polyps and normal nasal mucosa in upper airways. Currently, there are no detailed tissue distribution data pertaining to NLPR3 in BALB/c mice.…”

Section: Discussionmentioning

confidence: 99%

Tissue-specific expression of the NOD-like receptor protein 3 in BALB/c mice

Huang

Tong

et al. 2014

J Vet Sci

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Activation of the innate immune system requires recognition of pathogen-associated molecular patterns, such as NOD-like receptors. The NOD-like receptor protein 3 (NLRP3) inflammasome is involved in induction of the pro-inflammatory cytokine, IL-1β, and subsequent inflammatory responses. NLRP3 inflammasome plays important roles in the inflammatory and innate immune responses associated with autoimmune/inflammatory syndrome. However, analysis of the tissue distribution and expression profiles in BALB/c mice is still incomplete. In this study, we investigated the tissue distribution and expression pattern of NLRP3 in BALB/c mice to further elucidate its function in innate immunity in this commonly used laboratory animal model. NLRP3 mRNA expression levels and tissue distribution of the protein were investigated by real-time quantitative PCR and immunohistochemical analyses, respectively. NLRP3 mRNA expression was higher in the kidney and inguinal lymph nodes than in other tissues. Cytoplasmic expression of NLRP3 was detected in the epithelial reticular cells of the spleen and thymus, lymphocytes in the inguinal lymph nodes, cardiac muscle cells, cerebral cortex neurons, alveolar macrophages, renal tubule cells and liver sinusoidal endothelial cells. The results of this study will assist investigators in interpreting site-specific functions and roles of NLRP3 in inflammatory responses.

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“…These NLR receptors (NOD-like receptors) are found within the cytoplasm of cells and can also be triggered by microbial-derived factors [1]. Three of these receptors (NOD-1, NOD-2, and NALP-3) were investigated in NP and were shown to be highly enriched in the epithelia of patients relative to healthy controls and shown to be downregulated by steroid treatment [27]. In addition to the NLR class of receptors, an as-yet-unknown receptor is held responsible for the detection and responsiveness of airway epithelia to chitin [28].…”

Section: Chronic Rhinosinusitis and The Outside Microbial Worldmentioning

confidence: 99%

“…This would tie in with the observation that epithelial cells isolated from nonresponsive polyps (return of visible polyps within 6 months after surgery despite postoperative use of local and oral steroids) showed higher basal mRNA levels of IL-33 than epithelial cells isolated from responsive polyps [25, 62]. Moreover, reports show that downstream of ILC2s, CRS with NP is associated with lower levels of expression of the epithelial IL-22 receptor compared with healthy individuals or CRS patients without NP [63], and that polymorphisms in the gene are correlated with disease severity [27]. Given the ability of nasal epithelial cells to respond to IL-13 and IL-22, such a potential should consider that IL-33 can also be produced by fibroblasts and that IL-33 receptors can also be found on mast cells, eosinophils, and Th2 lymphocytes [12].…”

Section: A New View On Innate Immunity and Chronic Rhinosinusitismentioning

confidence: 99%

Role of Innate Immunity in the Pathogenesis of Chronic Rhinosinusitis: Progress and New Avenues

Drunen

Mjösberg

Segboer

et al. 2012

Curr Allergy Asthma Rep

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Chronic rhinosinusitis is a heterogeneous and multifactorial disease with unknown etiology. Aberrant responses to microorganisms have been suggested to play a role in the pathophysiology of the disease. Research has focused on the presence, detection, response to, and eradication of these potential threats. Main topics seem to center on the contribution of structural cells such as epithelium and fibroblasts, on the consequences of activation of pattern-recognition receptors, and on the role of antimicrobial agents. This research should be viewed not only in the light of a comparison between healthy and diseased individuals, but also in a comparison between patients who do or do not respond to treatment. New players that could play a role in the pathophysiology seem to surface at regular intervals, adding to our understanding (and the complexity) of the disease and opening new avenues that may help fight this incapacitating disease.

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NOD-like receptors in the human upper airways: a potential role in nasal polyposis

Abstract: The present study demonstrates the presence of NLRs in several upper airway tissues and highlights a potential role of NLRs in chronic rhinosinusitis with polyps.

Cited by 39 publications

References 35 publications

Immunolocalization of NLRP3 Inflammasome in Normal Murine Airway Epithelium and Changes following Induction of Ovalbumin-Induced Airway Inflammation

Immunolocalization of NLRP3 Inflammasome in Normal Murine Airway Epithelium and Changes following Induction of Ovalbumin-Induced Airway Inflammation

Tissue-specific expression of the NOD-like receptor protein 3 in BALB/c mice

Role of Innate Immunity in the Pathogenesis of Chronic Rhinosinusitis: Progress and New Avenues

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