Prostaglandin E2 suppresses staphylococcal enterotoxin–induced eosinophilia-associated cellular responses dominantly through an E-prostanoid 2–mediated pathway in nasal polyps

Okano, Mitsuhiro; Fujiwara, Tazuko; Tamano, Haruna; Kariya, Shin; Makihara, Seiichiro; Higaki, Toru; Nishizaki, Kazunori

doi:10.1016/j.jaci.2009.01.047

Cited by 51 publications

(55 citation statements)

References 46 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Because the effect of PGE 2 was mimicked by a selective prostanoid EP2 receptor agonist, it was suggested that PGE 2 , through EP2 receptors, inhibits the pathogenesis of SEB-induced eosinophilic inflammation. 22 Staphylococcal enterotoxins can thus have an additional amplifying role in upper airway disease by inhibiting the anti-inflammatory effect that PGE 2 might have through EP2 receptor activation. Because the latter mechanism in dispersed nasal polyp cells did not occur in the absence of diclofenac, it can be suggested that endogenous levels of constitutively produced PGE 2 are to some extent able to suppress the inflammatory response.…”

Section: Role Of Eicosanoids and Their Receptorsmentioning

confidence: 99%

Pathogenesis of chronic rhinosinusitis: Inflammation

Crombruggen¹,

Zhang²,

Gevaert³

et al. 2011

Journal of Allergy and Clinical Immunology

320

292

View full text Add to dashboard Cite

Section: Role Of Eicosanoids and Their Receptorsmentioning

confidence: 99%

Pathogenesis of chronic rhinosinusitis: Inflammation

Crombruggen¹,

Zhang²,

Gevaert³

et al. 2011

Journal of Allergy and Clinical Immunology

320

292

View full text Add to dashboard Cite

“…NPs were sampled during the endoscopic sinus surgery and then treated by enzymatic digestion using 2.0 mg/ml protease, 1.5 mg/ml collagenase, 0.75 mg/ml hyaluronidase, and 0.05 mg/ml DNase (all from Sigma, St. Louis, Mo., USA), as per a previously described method [5]. The study was preapproved by the Human Research Committee of the Okayama University Graduate School of Medicine and Dentistry, and all patients provided informed consent prior to their participation.…”

Section: Methodsmentioning

confidence: 99%

“…It is currently thought that NP formation affects between 1 and 4% of the population [2]. While the precise etiology and pathophysiology underlying CRS remains poorly understood, it has been proposed that networks of Th1, Th2, Th17, and Treg-associated cytokines might be involved [4,5,6,7]. …”

Section: Introductionmentioning

confidence: 99%

“…We compared the local expression of IL-18 among the various CRS phenotypes and examined the characterization of IL-18 expression in the pathogenesis of CRS. We further investigated not only the regulation of the local IL-18 release but also the regulatory effect of IL-18 on Th1/Th2/Th17-associated cytokine production in NPs using a recently developed ex vivo system [5,7]. The present findings provide novel insights into the pathogenesis of chronic eosinophilic airway diseases regulated by IL-18, in addition to providing a basis for the role of danger signals in IL-18 release in the airways [25].…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Characterization of IL-18 Expression and Release in the Pathogenesis of Chronic Rhinosinusitis

Okano

Fujiwara

Makihara

et al. 2012

Int Arch Allergy Immunol

Self Cite

View full text Add to dashboard Cite

Background: Interleukin-18 (IL-18) is a member of the IL-1 cytokine family that affects chronic inflammation. We sought to characterize IL-18 expression and investigate its release during chronic rhinosinusitis (CRS). Methods: The expression of IL-18 in nasal polyps (NPs) and uncinate tissues (UTs) from both CRS and non-CRS patients was examined via immunohistochemistry. After culturing dispersed NP cells (DNPCs) with or without various stimulations, IL-18 levels were measured in the culture supernatants. Furthermore, the effect of IL-18 neutralization on staphylococcus enterotoxin B (SEB)-induced cytokine production was also examined. Results: Similar expression of IL-18 in the epithelial layers was observed between the NPs and UTs. However, there was a significantly higher number of IL-18⁺ cells in the lamina propria from NPs compared to UTs without CRS. This increased number was significantly correlated with the radiological severity of sinusitis and local eosinophilia. After the dispersion, IL-18 was spontaneously released by NP cells in a phase-dependent manner. While SEB, fungal antigens, and TLR agonists did not enhance the release, exposure to protease or one cycle of a freeze-and-thaw treatment did induce release of IL-18 from rested DNPCs. In addition, neutralization of IL-18 significantly suppressed SEB-induced IL-5, IL-13, and IFN-γ, but not IL-17A production. Conclusions: These results suggest that the pro-inflammatory effect of IL-18 released by danger signals may be involved in the pathogenesis of CRS, which includes eosinophilic inflammation and NP formation, via the augmentation of both Th2- and Th1-associated cytokine production.

show abstract

“…53,80,81 Since environmental microbes such as Staphylococcus aureus and fungi can evoke eosinophilia-associated cellular responses in sinonasal mucosa in patients with CRSwNP, nasal saline irrigation is also recommended. 58,82,83 In terms of antibiotics, doxycycline showed a substantial effect on ECRS including on polyp size and ECP levels in nasal secretions whereas the effect of 14-ring macrolides on ECRS is poor. 81,84 Since biofilm is also known to be an intractable factor in the pathogenesis of CRS, the efficacy and safety of topical antibiofilm agents such as surfactants and manuka honey have also been investigated.…”

Section: Effect Of Intervention For Chronic Rhinosinusitis On Asthmamentioning

confidence: 99%

Association and management of eosinophilic inflammation in upper and lower airways

Okano

Kariya

Ohta

et al. 2015

Allergology International

Self Cite

View full text Add to dashboard Cite

This review discussed the contribution of eosinophilic upper airway inflammation includes allergic rhinitis (AR) and chronic rhinosinusitis (CRS) to the pathophysiology and course of asthma, the representative counterpart in the lower airway. The presence of concomitant AR can affect the severity of asthma in patients who have both diseases; however, it is still debatable whether the presence of asthma affects the severity of AR. Hypersensitivity, obstruction and/or inflammation in the lower airway can be detected in patients with AR without awareness or diagnosis of asthma, and AR is known as a risk factor for the new onset of wheeze and asthma both in children and adults. Allergen immunotherapy, pharmacotherapy and surgery for AR can contribute to asthma control; however, a clear preventive effect on the new onset of asthma has been demonstrated only for immunotherapy. Pathological similarities such as epithelial shedding are also seen between asthma and CRS, especially eosinophilic CRS. Abnormal sinus findings on computed tomography are seen in the majority of asthmatic patients, and asthmatic patients with CRS show a significant impairment in Quality of Life (QOL) and pulmonary function as compared to those without CRS. Conversely, lower airway inflammation and dysfunction are seen in non-asthmatic patients with CRS. Treatments for CRS that include pharmacotherapy such as anti-leukotrienes, surgery, and aspirin desensitization show a beneficial effect on concomitant asthma. Acting as a gatekeeper of the united airways, the control of inflammation in the nose is crucial for improvement of the QOL of patients with co-existing AR/CRS and asthma.

show abstract

Prostaglandin E2 suppresses staphylococcal enterotoxin–induced eosinophilia-associated cellular responses dominantly through an E-prostanoid 2–mediated pathway in nasal polyps

Cited by 51 publications

References 46 publications

Pathogenesis of chronic rhinosinusitis: Inflammation

Pathogenesis of chronic rhinosinusitis: Inflammation

Characterization of IL-18 Expression and Release in the Pathogenesis of Chronic Rhinosinusitis

Association and management of eosinophilic inflammation in upper and lower airways

Contact Info

Product

Resources

About