Superantigens and nasal polyps

Bachert, Claus; Zele, Thibaut Van; Gevaert, Philippe; Schrijver, L. De; Cauwenberge, Paul Van

doi:10.1007/s11882-003-0065-y

Cited by 86 publications

(102 citation statements)

References 82 publications

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“…Multiple groups have proposed that CRS results from an abnormal immune response to microorganisms or their products, including fungi, Staphylococci, Pseudomonal biofilms, or viruses. [22][23][24][25][26][27][28][29] Innocuous or ubiquitous agents do not ordinarily generate a vigorous immune response in healthy hosts, and normal mucosal immune activity against potential microbial pathogens typically involves elaboration of innate immune effectors and Th1-like inflammatory mediators. In CRSwNP, the mucosal immune abnormality appears to be twofold: on the one hand, there is a failure to prevent or eliminate microbial colonization of the sinonasal cavities, and on the other hand, there is a seemingly inappropriate Th2-biased immune response perpetuated within the mucosa.…”

Section: Discussionmentioning

confidence: 99%

Th2 Cytokines associated with Chronic Rhinosinusitis with Polyps Down-Regulate the Antimicrobial Immune Function of Human Sinonasal Epithelial Cells

Ramanathan

Lee

Spannhake

et al. 2008

American Journal of Rhinology

104

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Background-Chronic rhinosinusitis with nasal polyps (CRSwNPs) is a disorder characterized by persistent eosinophilic Th2 inflammation and frequent sinonasal microbial colonization. It has been postulated that an abnormal mucosal immune response underlies disease pathogenesis. The relationship between Th2 inflammatory cytokines and the innate immune function of sinonasal epithelial cells (SNECs) has not been explored.

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Section: Discussionmentioning

confidence: 99%

Th2 Cytokines associated with Chronic Rhinosinusitis with Polyps Down-Regulate the Antimicrobial Immune Function of Human Sinonasal Epithelial Cells

Ramanathan

Lee

Spannhake

et al. 2008

American Journal of Rhinology

104

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“…However, the events that trigger nasal polyp formation have not been fully described. A variety of microorganisms and microbial products have been proposed, but no single agent has been proven to play a causative role [1,2]. Fungal disease of the sinuses has been recognized since 1981, and was once considered rare [3].…”

Section: Introductionmentioning

confidence: 99%

Airborne Fungi Induce Nasal Polyp Epithelial Cell Activation and Toll-Like Receptor Expression

Shin

Lee²

2010

Int Arch Allergy Immunol

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Background: The nasal epithelium is the first barrier encountered by airborne allergens and is an active participant in airway inflammation. Fungi have been increasingly recognized as important pathogens in sinusitis and airway diseases. The aim of the study was to evaluate fungal protease activity during cytokine production in nasal polyp epithelial cells and to determine the expression of Toll-like receptor (TLR) mRNA by fungi. Methods: Nasal polyp epithelial cells were obtained from patients and stimulated with Alternaria and Aspergillus. Interleukin-8 (IL-8) and granulocyte macrophage colony-stimulating factor (GM-CSF) were measured to determine the activation of epithelial cells. Reverse transcriptase polymerase chain reaction for the TLR mRNA expression of the nasal epithelial cells was performed. Cytokine production was inhibited with protease inhibitors and anti-human TLR antibodies. Results: The fungi enhanced the production of IL-8 and GM-CSF from nasal epithelial cells. When nasal epithelial cells were activated by the fungi, TLR2, TLR3 and TLR4 mRNAs were more strongly expressed than in the nonactivated cells. Cytokine production was inhibited by protease inhibitors and anti-human TLR4 antibodies. Conclusions: The results of this study showed that fungi interacted with nasal epithelial cells and enhanced the production of cytokines and TLR mRNA expression. The cytokine production was related to the protease in fungi and TLR4.

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“…In a Dutch study, Brosens et al (2005) reported that the polymorphism -765G/C of COX-2 gene was significantly higher in the normal-appearing mucosa of patients with familial adenomatous polyposis (Petruson et al, 1988). However, Huuskonen et al (2008) demonstrated that the functional C variant of the -765G/C polymorphism in the human COX-2 gene associates with the severity of coronary atherosclerosis measured at the coronary artery level in Finnish population (Bachert et al, 2003). Little data evidenced an association between nose polyps and this polymorphism.…”

Section: Discussionmentioning

confidence: 99%

“…Moreover, Zhang et al (2005) reported that the -765GC genotype was associated with an increased risk of esophageal squamous cell carcinoma and CRC in Chinese population (Weidner et al, 1993). Xing et al (2008) showed that the COX-2-765G/ C allele promoter polymorphism is significantly associated with colorectal cancer risk (Bachert et al, 2003). In addition, the -765GC and 765CC genotypes correlate with decreased risk of myocardial infarct and stroke and decreased COX-2 expression in atherosclerotic plaques compared with -765GG (Coste et al, 2000).…”

Section: Discussionmentioning

confidence: 99%

“…Mucosal eosinophilic inflammation is the ground on which easily arise, in particular, nasal polyps. Much less chronic rhinosinusitis with nasal polyps proceeds from the domination of the neutrophil infiltration in inflammatory mucosa of the nose and paranasal sinuses (Bachert et al, 2003). Although the role of allergy in chronic rhinosinusitis remains controversial, it has been postulated that the swelling of the nasal mucosa in allergic rhinitis may restrict ventilation and obstruct the sinus ostia, leading to mucus retention and an infection (Fokkens et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

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Association of the −14C/GMETand the −765G/CCOX-2Gene Polymorphisms with the Risk of Chronic Rhinosinusitis with Nasal Polyps in a Polish Population

Sitarek

Zielińska‐Bliźniewska

Dziki

et al. 2012

DNA and Cell Biology

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Chronic rhinosinusitis with nasal polyps is strongly associated with other diseases, including asthma and allergy. The following study tested the association of the -765G/C polymorphism of cyclooxygenase-2 (COX-2) encoding gene and the -14C/G polymorphism of protooncogen MET (MET) encoding gene with a risk of chronic rhinosinusitis with nasal polyps in a Polish population. One hundred ninety-five patients of chronic rhinosinusitis with nasal polyps as well as 200 sex-, age-, and ethnicity-matched control subjects without chronic sinusitis and nasal polyps were enrolled in this study. Among the group of patients, 63 subjects were diagnosed with allergy and 65 subjects with asthma, respectively. DNA was isolated from peripheral blood lymphocytes of patients as well as controls, and gene polymorphisms were analyzed by restriction fragment length polymorphism-polymerase chain reaction (RFLP-PCR). Ten percent of the samples have been confirmed by a second method single-strand conformation polymorphism (SSCP)-PCR. We reported that the -765G/C COX-2 (odds ratio [OR] 7.79; 95% confidence interval [CI] 4.88-12.4, p < 0.001) and the -14C/G MET (OR 2.83; 95% CI 1.74-4.61, p < 0.001) were associated with an increased risk of chronic rhinosinusitis with nasal polyps among analyzed group of patients. Moreover, the group of patients without allergy or asthma indicated the association of the -765C/G (OR 7.25; 95% CI 4.38-12.1, p < 0.001 and OR 7.61; 95% CI 4.47-12.6, p < 0.001) genotype of the COX-2 as wells as the -14C/G (OR 2.47; 95% CI 1.46-4.17, p < 0.001 and OR 2.59; 95% CI 1.54-4.37, p < 0.001) genotype of MET with an increased risk of chronic rhinosinusitis with nasal polyps. Finally, it was also found that the selected group of patients with allergy or asthma indicated a very strong association of the -765G/C (OR 5.64;.03, p < 0.001, respectively) genotype of the COX-2 with an increased risk of chronic rhinosinusitis with nasal polyps. Thus, our results suggest that COX-2 and MET gene polymorphisms may have deep impact on the risk of rhinosinusitis nasal polyp formation, which may also depend on asthma or allergy. Our results showed that the -765G/C polymorphism of COX-2 gene and the -14C/G polymorphism of the MET gene may be associated with the risk of chronic rhinosinusitis with nasal polyps in a Polish population.

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Superantigens and nasal polyps

Cited by 86 publications

References 82 publications

Th2 Cytokines associated with Chronic Rhinosinusitis with Polyps Down-Regulate the Antimicrobial Immune Function of Human Sinonasal Epithelial Cells

Th2 Cytokines associated with Chronic Rhinosinusitis with Polyps Down-Regulate the Antimicrobial Immune Function of Human Sinonasal Epithelial Cells

Airborne Fungi Induce Nasal Polyp Epithelial Cell Activation and Toll-Like Receptor Expression

Association of the −14C/GMETand the −765G/CCOX-2Gene Polymorphisms with the Risk of Chronic Rhinosinusitis with Nasal Polyps in a Polish Population

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