Effects of Glucocorticoids on Infiltrating Cells and Epithelial Cells of Nasal Polyps

Watanabe, Kazumasa; Kanaizumi, Etsuko; Shirasaki, Hideaki; Himi, Tetsuo

doi:10.1177/000348940411300610

Cited by 31 publications

(27 citation statements)

References 36 publications

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“…It has been reported that in lower airway diseases (e.g., asthma, bronchiolitis obliterans, chronic obstructive pulmonary disease, and cystic fibrosis), the pseudostratified airway surface epithelium is severely damaged and must regenerate to restore its defense functions [11]. The same results have also been found in the sinonasal epithelial cells from CRSwNP, such as up-regulation of MUC1, MUC4, and MUC8 [12,13]; down-regulation of MUC5AC [12,13] and TLR9 [14]; upexpression of VPF/VEGF [15,16] and LL-37 [17,18]; increased production of GM-CFS [19]; and staph invasion of sinonasal epithelial cells [20]. It is interesting that during the recovery or resolution phase of viral infections in the lower airways, the immune system must help to orchestrate tissue repair to restore normal lung architecture and function and prevent permanent defects in respiratory function [4••].…”

Section: Role Of Nasal Epithelium In Common Upper Airway Diseasesmentioning

confidence: 73%

Upper Airway Stem Cells: Understanding the Nose and Role for Future Cell Therapy

Wang

Yan

et al. 2014

Curr Allergy Asthma Rep

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The nose together with the paranasal sinuses has an approximate surface area of 100 to 200 cm(2) in adults, which is lined with pseudostratified columnar ciliated epithelium. It serves several important physiological functions such as conditioning and filtration of the inspired air and the provision of end organ for the sense of smell. It is also a physical and immunological barrier as it is the first site of interaction between the host tissue and foreign invaders (viruses, bacteria, and allergens). Our understanding of the complex cellular events occurring in response to inhaled agents during the development of common airway diseases has been significantly enhanced by the current status of in vivo and in vitro nasal experimental models. This will allow the development of novel therapeutic strategies designed to improve the physiological and immune defense functions of the nasal epithelium, as well as novel therapies for other common nasal diseases.

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Section: Role Of Nasal Epithelium In Common Upper Airway Diseasesmentioning

confidence: 73%

Upper Airway Stem Cells: Understanding the Nose and Role for Future Cell Therapy

Wang

Yan

et al. 2014

Curr Allergy Asthma Rep

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“…There are a few studies to determine the effect of glucocorticoids on apoptosis in nasal polyps [4,5,6]. However, these studies only identified the induction of apoptosis in the stromal cells, fibroblasts, eosinophils and T lymphocytes in nasal polyps by glucocorticoids in vitro .…”

Section: Discussionmentioning

confidence: 99%

“…Glucocorticoids increased apoptosis in a variety of polymorphonuclear cells, such as eosinophils, T lymphocytes and fibroblasts in nasal polyps [5,6]. The mechanism of glucocorticoids-induced apoptosis performed in lymphoid cells, like thymocytes, has been identified through in vitro studies, however the exact signaling pathway for glucocorticoids induced apoptosis in nasal polyp remains unclear.…”

Section: Introductionmentioning

confidence: 99%

Dexamethasone Induces Apoptosis of Nasal Polyp-Derived Tissue Cultures Through JNK and p38 MAPK Activation

Lee

Nam

Lee

et al. 2014

Clin Exp Otorhinolaryngol

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ObjectivesGlucocorticoids, such as dexamethasone (DEX), increase apoptosis in a variety of white cells in nasal polyps and apoptosis is an important factor in the resolution of inflammation. However, the mechanism of glucocorticoids induced apoptosis in nasal polyp remains unclear. In this study the authors evaluated which pathways were engaged in apoptosis induced by DEX in an ex vivo model of nasal polyps.MethodsNasal polyp tissues were cultured using an air-liquid interface method. Cultures were maintained in the absence or presence of DEX (10 or 100 µM) for 24 hours. To investigate the involvement of the apoptotic signaling pathways in nasal polyp, such as caspase cascades, Fas-FasL signaling pathway, mitochondrial pathway and p38 mitogen-activated protein kinase (MAPK)/JNK pathway, the authors performed reverse transcription-polymerase chain reaction and Western blotting.ResultsThe expression ratios of FasL, activated form of caspase-8, caspase-9, and caspase-3 were significantly higher in DEX-treated polyps (P<0.01). In the Bcl-2 family expression, the anti-apoptotic molecules, Bcl-2 and Bcl-XL decreased, but pro-apoptotic molecules, Bax increased, and Bid and Bad were activated. In the conventional MAPKs, JNK, and the phospho-p38 MAPK were significantly higher, but phospho-extracellular signal-regulated kinase (ERK)1/2 was significantly lower in DEX-treated polyps (P<0.01).ConclusionDEX induces apoptosis of nasal polyp via caspase cascades, Fas-FasL signaling pathway, mitochondrial pathway and p38 MAPK/JNK pathway.

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“…On the other hand, Hamilos et al 15 noted a marked decrease in GM-CSF, but not in TNF-α, in an in vivo study of fluticasone use during one month. Watanabe et al 11 also found decreased GM-CSF levels in nasal polyp epithelial cells under GC therapy, which would explain reduced eosinophil apoptosis.…”

Section: Gc Intracellular Action and On Inflammatory Mediatorsmentioning

confidence: 93%

Mecanismos de ação dos corticosteróides na polipose rinossinusal

Fernandes¹,

Valera²,

Anselmo‐Lima³

2008

Rev. Bras. Otorrinolaringol.

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Os glicocorticóides (GC) são drogas de escolha no tratamento clínico da polipose nasossinusal conforme recomendação da literatura. Entretanto, seus mecanismos de ação nas regressões dos sintomas clínicos e dos pólipos não são totalmente compreendidos. Sabe-se que a administração tópica e ou sistêmica dos glicocorticóides leva a variações na expressão de citocinas, quimiocinas e linfocinas, além das alterações celulares. Assim, os GC suprimem a expressão de citocinas pró-inflamatórias, de quimiocinas, de moléculas de adesão, além de estimular a transcrição de citocinas antiinflamatórias. Citocinas pró-fibróticas como a IL-11, fator básico de crescimento do fibroblasto (b-FGF) e fator de crescimento endotelial vascular (VEGF), relacionados com o crescimento do pólipo, também são suprimidos pela ação do GC. Tal ação depende fundamentalmente da interação com os seus receptores (GR), pois alguns indivíduos apresentam algum grau de resistência celular ao seu efeito, que parece estar relacionada com a presença da isoforma <FONT FACE=Symbol>b</font> do GR. Genes envolvidos nas fases de produção de imunoglobulinas, apresentação e processamento do antígeno também sofrem ação dos GC de forma variada. OBJETIVOS: Fazer uma revisão da literatura sobre os mecanismos de ação do GC na PNS. CONCLUSÃO: A compreensão desses mecanismos implicará no desenvolvimento de drogas mais eficazes na sua terapêutica.

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Effects of Glucocorticoids on Infiltrating Cells and Epithelial Cells of Nasal Polyps

Cited by 31 publications

References 36 publications

Upper Airway Stem Cells: Understanding the Nose and Role for Future Cell Therapy

Upper Airway Stem Cells: Understanding the Nose and Role for Future Cell Therapy

Dexamethasone Induces Apoptosis of Nasal Polyp-Derived Tissue Cultures Through JNK and p38 MAPK Activation

Mecanismos de ação dos corticosteróides na polipose rinossinusal

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