Total and specific IgE in nasal polyps is related to local eosinophilic inflammation

Bachert, Claus; Gevaert, Philippe; Holtappels, Gabriële; Johansson, S. G. O.; Cauwenberge, Paul Van

doi:10.1067/mai.2001.112374

Cited by 593 publications

(589 citation statements)

References 36 publications

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“…The correlations of ECP, IL5 and IgE confirm previous data in Caucasian nasal polyps, where inflammation is dominated by activated eosinophils 15 and IgE concentrations were related to eosinophilic inflammation 21 . The association of albumin with eosinophil products can be related to observations in nasal polyps where increased albumin deposition has been thought to be caused by eosinophil-driven inflammation 15 .…”

Section: Discussionsupporting

confidence: 77%

Inflammatory endotypes of chronic rhinosinusitis based on cluster analysis of biomarkers

Tomassen

Vandeplas

Zele

et al. 2016

Journal of Allergy and Clinical Immunology

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859

878

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Section: Discussionsupporting

confidence: 77%

Inflammatory endotypes of chronic rhinosinusitis based on cluster analysis of biomarkers

Tomassen

Vandeplas

Zele

et al. 2016

Journal of Allergy and Clinical Immunology

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859

878

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“…Recent reports of high levels of IgE in nasal polyp tissue suggest that IgE may be generated locally against one or more aeroallergens. A subgroup of nasal polyposis patients with specific IgE to staphylococcal enterotoxins has been defined [10], pointing to the possibility that bacterial superantigens may drive the non-seasonal eosinophilic inflammation that is a hallmark of nasal polyps [1][2][3]. It is not known whether such a mechanism is common to patients with and without aspirin intolerance.…”

Section: Discussionmentioning

confidence: 99%

Specific immunoglobulin E for staphylococcal enterotoxins in nasal polyps from patients with aspirin‐intolerant asthma

Suh

Yoon

Sampson

et al. 2004

Clin Experimental Allergy

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SummaryBackground Nasal polyps infiltrated with eosinophils are commonly found in chronic asthmatic patients, more frequently in those with aspirin-intolerant asthma (AIA) than aspirin-tolerant asthma (ATA). Some studies have suggested a contribution of superantigens derived from Staphylococcus sp to nasal polyposis and eosinophilia, but their relative importance in AIA and ATA subjects is unknown. Objective We investigated whether local production of specific IgE to staphylococcal enterotoxins A and B (SEA and SEB) and relationships with markers of eosinophilic inflammation differ in the nasal polyps of AIA and ATA subjects. Methods Fifteen AIA subjects with positive responses to lysine-aspirin bronchoprovocation and 15 ATA subjects underwent polypectomy. Immunoassays were used to quantify eosinophil cationic protein (ECP), IL-5, mast cell tryptase, soluble IL-2 recepters (sIL-2R), total IgE, and specific IgE for SEA and SEB. Results ECP levels in nasal polyp homogenates were higher in AIA subjects than in ATA subjects (Po0.02), with no significant differences in tryptase, IL-5 or sIL-2R. Total IgE, and specific IgE to both SEA and SEB, were detectable in some nasal polyps from both subject groups, but median levels were markedly higher in AIA subjects than in ATA subjects (P 5 0.04, 0.01, 0.05, respectively). Levels of specific IgE to SEA and SEB correlated significantly with levels of ECP and IL-5, but not those of tryptase or sIL-2R. Conclusion These findings suggest that staphylococcal superantigens may drive local eosinophilic inflammation in nasal polyp tissue, and that this is exacerbated in subjects with AIA.

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“…All adenoid and tonsillar tissue specimens (n ϭ 20 for SA group, n ϭ 9 for RI group) were processed as described by Bachert and colleagues (38). In brief, tissues were weighed, and 1 ml of 0.9% NaCl solution was added per 0.1 g of tissue.…”

Section: Lt Concentrationsmentioning

confidence: 99%

Leukotriene Modifier Therapy for Mild Sleep-disordered Breathing in Children

Goldbart

Goldman

Veling

et al. 2005

Am J Respir Crit Care Med

279

156

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Background: Children with mild sleep-disordered breathing (SDB), who may not be recommended for adenotonsillectomy, frequently exhibit neurocognitive and behavioral morbidity, and may benefit from alternative therapeutic interventions, such as leukotriene modifier therapy. Methods: Twenty-four children with SDB completed an open-label intervention study for 16 weeks with daily montelukast therapy. Sleep studies and adenoid size estimates from lateral X-ray films of the neck were obtained before and after treatment. In a parallel study, adenoid and tonsillar tissues from children with obstructive sleep apnea or recurrent throat infections were subjected to quantitative polymerase chain reaction, immunohistochemistry, and Western blotting for gene and protein expression of leukotriene receptors LT1-R and LT2-R, and for concentrations of LTB4 and LTC4/D4/E4. Results: Montelukast treatment induced significant reductions in adenoid size and respiratory-related sleep disturbances, which were absent in 16 children with SDB who did not receive treatment. LT1-R and LT2-R mRNA was similarly abundant in adenoid tissues, but increased LT1-R and LT2-R protein expression and higher levels of LTB4 and LTC4/D4/E4 emerged in children with obstructive sleep apnea. Conclusions: Oral therapy with a leukotriene modifier appears to be associated with improved breathing during sleep. Double-blind, placebo-controlled trials will be needed to corroborate current findings and solidly establish antiinflammatory strategies, such as leukotriene modifiers, as therapeutic alternatives in children with SDB too mild to justify referral for adenotonsillectomy.

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Total and specific IgE in nasal polyps is related to local eosinophilic inflammation

Cited by 593 publications

References 36 publications

Inflammatory endotypes of chronic rhinosinusitis based on cluster analysis of biomarkers

Inflammatory endotypes of chronic rhinosinusitis based on cluster analysis of biomarkers

Specific immunoglobulin E for staphylococcal enterotoxins in nasal polyps from patients with aspirin‐intolerant asthma

Leukotriene Modifier Therapy for Mild Sleep-disordered Breathing in Children

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