Role of Interleukins and Transforming Growth Factor-β in Chronic Rhinosinusitis and Nasal Polyposis

Bradley, Dewayne T.; Kountakis, Stilianos E.

doi:10.1097/01.mlg.0000161334.67977.5d

Cited by 46 publications

(37 citation statements)

References 17 publications

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“…[13] On the other hand, a variety of other cytokines like IL-6, IL-8, IL-11, IL-16 are nonspecific markers of the inflammation in these patients. [14,15] IL-16 is a highly potent chemotactic and chemoattractant molecule for eosinophils. Lackner et al [15] reported a local increase of IL-16 in nasal polyp tissue.…”

Section: Discussionmentioning

confidence: 99%

Red blood cell distribution width in patients with nasal polyposis

Topal¹

2017

Kulak Burun Bogaz Ihtis Derg

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Objectives: This study aims to evaluate the red blood cell distribution width (RDW) levels of patients with nasal polyposis (NP), and investigate its value as an inflammatory parameter and possible correlation with the severity of the disease. Patients and Methods:Between January 2003 and September 2016, a total of 139 NP patients (87 males, 52 females; mean age 46.6 years; range 22 to 87 years) and 80 controls (59 males, 21 females; mean age 30.3 years; range 17 to 64 years), who underwent nasal septal reconstruction surgery, were included in this retrospective controlled study. Data including polyp stage, computed tomography (CT) score, number of eosinophils in peripheral blood, total serum immunoglobulin E (IgE) and RDW were obtained from medical records.Results: Red blood cell distribution width was above normal values in 56 NP patients (40.28%). Mean RDW was 15.3906±1.41805% in NP group and 14.6413±0.83191% in the control group. The difference was statistically significant between the two groups (p<0.001). There was no statistically significant correlation between RDW and total serum IgE, number of total eosinophils in peripheral blood, polyp stage, and CT scores. Conclusion:Patients with NP showed significantly increased RDW values compared to controls. Although we failed to demonstrate an association of elevated RDW with the disease severity, this preliminary study may give rise to further prospective studies.Keywords: Inflammation; nasal polyp; red blood cell distribution width. Sonuç: Nazal polipli hastalar, kontrol grubu ile karşılaştırıldığında KKDG değerlerinde anlamlı olarak artış gösterdi. Yüksek KKDG değerlerinin hastalık şiddeti ile ilişkisi ortaya konmamış olsa da, bu ön çalışma ileriye yönelik prospektif çalışmalara yol gösterici olabilir. Department of OtolaryngologyAnahtar Sözcükler: Enflamasyon; nazal polip; kırmızı kan hücresi dağılım genişliği.

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Section: Discussionmentioning

confidence: 99%

Red blood cell distribution width in patients with nasal polyposis

Topal¹

2017

Kulak Burun Bogaz Ihtis Derg

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“…IL-6 has been shown to enhance the differentiation of B cells and their consequent production of immunoglobulins. Furthermore, IL-6 has been reported to be a primary inducer of the acute-phase response [21][22][23]. It does not induce cytokine expression; therefore, its main effects are to augment the responses of immune cells like regulatory T cells to other cytokines [22].…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, IL-8 has a wide range of actions on various types of cells, including lymphocytes, monocytes, endothelial cells, and fibroblasts, besides neutrophils [32]. The discovery of these biological functions might suggest that IL-8 is also a marker of sinus inflammation in patients with CRS [21,33]. Beside others Bradley et al showed that IL-8 is a non-specific marker of sinus inflammation being expressed in patients with CRS and patients with CRS/NP [21,34].…”

Section: Discussionmentioning

confidence: 99%

“…The discovery of these biological functions might suggest that IL-8 is also a marker of sinus inflammation in patients with CRS [21,33]. Beside others Bradley et al showed that IL-8 is a non-specific marker of sinus inflammation being expressed in patients with CRS and patients with CRS/NP [21,34]. Furthermore, IL-8 may modulate remodeling in nasal polyps [35].…”

Section: Discussionmentioning

confidence: 99%

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Pro-inflammatory effects of ochratoxin A on nasal epithelial cells

Cremer

Soja

Sauer

et al. 2011

Eur Arch Otorhinolaryngol

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Eosinophilic chronic rhinosinusitis (ECRS) largely consists of allergic fungal sinusitis, non-allergic fungal rhinosinusitis, aspirin-exacerbated ECRS, and superantigen-induced ECRS. The pathophysiology of ECRS is not completely understood, in particular, the role of mycotoxins remains unknown. The aim of this study was to evaluate the effects of one of the most widespread mycotoxin, ochratoxin A (OTA), on the release of pro-inflammatory cytokines such as interleukin-(IL)-6 and the CXC-chemokine IL-8 from nasal epithelial cell cultures (NEC) of subjects with and without ECRS. NEC (ECRS group: n = 16; controls: n = 7) were stimulated with OTA for 24 h. Protein concentrations of IL-6 and IL-8 levels were measured in NEC supernatants by ELISA prior and 24 h after addition of OTA. Baseline levels in the supernatants of NEC were 183.3 pg/ml for IL-6 and 384.6 pg/ml for IL-8. Stimulation with OTA induced a significant increase of IL-6 (p < 0.001) and IL-8 (p < 0.001) in both NEC of controls and ECRS, respectively. There were no significant differences between controls and ECRS. This is the first study evaluating the effects of a mycotoxin on epithelial airway cells. Our data show that the ubiquitous mycotoxin OTA has a strong pro-inflammatory effect on NEC resulting in the release of IL-6 and IL-8. Mycotoxins may promote inflammation in nasal mucosa.

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“…The transcription of TGF-β was found to be 3.2 times greater in patients with chronic rhinosinusitis and nasal polyps than in patients with chronic rhinosinusitis alone. Moreover, patients with chronic rhinosinusitis and nasal polyps demonstrate increased transcription of the TGF-β gene in response to IL-4 treatment, suggesting that a Th2-mediated mechanism may be responsible for stromal proliferation and formation of nasal polyposis [38].…”

Section: Eosinophilsmentioning

confidence: 99%

Pathogenesis of nasal polyps: An update

Pawliczak

Lewandowska–Polak

Kowalski

2005

Curr Allergy Asthma Rep

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The cause of nasal polyp formation is still unknown. Genetic predisposition has been suggested, but there are scanty data to support such theories. Activated epithelial cells may be the major source of mediators inducing influx of inflammatory cells (mostly eosinophils) and proliferation and activation of fibroblasts leading to nasal polyp formation. Infectious agents (including viruses, bacteria, or fungi) may be potential primary factors activating nasal epithelial cells. Proinflammatory cytokines and growth factors play important roles in the persistence of mucosal inflammation associated with nasal polyps. Arachidonic acid metabolites seem to be particularly important in the pathogenesis of nasal polyps in patients with aspirin hypersensitivity rhinosinusitis/asthma syndrome.

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Role of Interleukins and Transforming Growth Factor-β in Chronic Rhinosinusitis and Nasal Polyposis

Cited by 46 publications

References 17 publications

Red blood cell distribution width in patients with nasal polyposis

Red blood cell distribution width in patients with nasal polyposis

Pro-inflammatory effects of ochratoxin A on nasal epithelial cells

Pathogenesis of nasal polyps: An update

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