In vitro effect of glucocorticoids on nasal polyps

Valera, Fabiana Cardoso Pereira; Brassesco, María Sol; Castro‐Gamero, Angel Mauricio; Cortez, María Angélica; Queiróz, Rosane Gomes de Paula; Tone, Luíz Gonzaga; Anselmo‐Lima, Wilma Terezinha

doi:10.1590/s1808-86942011000500012

Cited by 4 publications

(3 citation statements)

References 23 publications

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“…This finding may be due to the therapeutic control being different between both patient groups, and as a consequence, the inflammation biomarkers are controlled in AERD; this result has been reported by Baraket et al, who demonstrated a decrease in TNF-α concentrations in a bronchioalveolar wash after treatment with inhaled fluticasone propionate in asthmatic patients [32]. Varela et al reported a similar finding in cultivating fibroblasts from nasal polyps, which, upon exposure to this steroid, inhibit the synthesis of cellular adhesion molecules [33]. In a similar model, Silvestri et al reported a decrease in the expression of ICAM-1, but not VCAM-1, in the presence of TNF-α [34].…”

Section: Discussionsupporting

confidence: 55%

Single nucleotide polymorphisms in TNF are associated with susceptibility to aspirin-exacerbated respiratory disease but not to cytokine levels: a study in Mexican mestizo population

Pavón-Romero

Reséndiz-Hernández

Ramírez-Jiménez

et al. 2017

Biomarkers in Medicine

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Aim:To evaluate the association of three single nucleotide polymorphisms in TNF and one in LTA in Mexican patients with aspirin-exacerbated respiratory disease (AERD) and the correlation of those single nucleotide polymorphisms with serum levels of TNF-α. Patients & methods: Case-control study including 133 patients with AERD, 135 patients with asthma (aspirin-tolerant asthmatics) and 182 healthy subjects. Results: GA genotype of rs1800629 in TNF was found to be associated with the risk of developing AERD (p < 0.05; odds ratio = 2.36) and by dominant model (p < 0.05; odds ratio = 2.51). Furthermore, there was a difference in the serum levels between the aspirin-tolerant asthmatics group and the other groups (p < 0.001). Conclusion: The GA genotype of rs1800629 is associated with genetic susceptibility to AERD, but it does not correlate to protein serum levels. Aspirin-exacerbated respiratory disease (AERD) is a clinical disease characterized by hypersensitivity to aspirin, asthma and chronic rhinosinusitis with nasal polyps. It affects 10% of the population with asthma; however, its prevalence increases to 21% when provocation tests are used [1]. AERD is a disease characterized by restructuring of the airway [2] and the presence of extensive hyperplastic eosinophilic sinusitis with the formation of nasal polyps [3]. The most important clinical characteristic is bronchoconstriction after the administration of aspirin (ASA) or other nonsteroidal anti-inflammatory drugs (NSAIDs) [2,4]. The physiopathology involves a block in the cyclooxygenase pathway that promotes a diversion of arachidonic acid metabolism toward the lipoxygenase pathway, inducing the synthesis of leukotrienes such as LTC4, LTD4 and LTE4 [5,6], proteins that induce inflammatory cell chemotaxis, and the release of cytokines such as TNF-α [7] and lymphotoxin. TNF-α is a critical molecule in the regulation of inflammation because it induces a cascade of other inflammatory cytokines, chemokines and growth factors [8]. The results of various in vivo and in vitro studies indicate that the increase in their production is involved in the severity of the inflammation, due to their participation in restructuring the airway and in the pro-oxidative response [9]. In relation to single nucleotide polymorphisms (SNPs), it has been reported that rs1800629 (G→A change in position -308) increases transcriptional activity [10,11], in addition to being associated with different pulmonary pathological diseases such as chronic obstructive pulmonary disease and asthma [9,12,13]. However, no SNPs have been reported in TNF or LTA that are associated with AERD.

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Section: Discussionsupporting

confidence: 55%

Single nucleotide polymorphisms in TNF are associated with susceptibility to aspirin-exacerbated respiratory disease but not to cytokine levels: a study in Mexican mestizo population

Pavón-Romero

Reséndiz-Hernández

Ramírez-Jiménez

et al. 2017

Biomarkers in Medicine

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“…The final effect of GC on nasal diseases is the inhibition of pro-inflammatory cytokines (IL-1 , TNF-, GM-CSF, IL-3, IL-5, IL-6), chemokines (IL-8, RANTES, eotaxin) and adhesion molecules (VCAM-1, ICAM-1) [1, 13,42]. Glucocorticoids also have a favorable effect on tissue remodeling (reducing MMP expression) [43,44], reduce mucin production [45], increase cell apoptosis [46,47], and decrease mast cell recruitment and activation [48].…”

Section: Glucocorticoid Action On Nasal Mucosamentioning

confidence: 99%

Glucocorticoid Resistance in the Upper Respiratory Airways

Valera¹,

Tamashiro²,

Anselmo‐Lima³

2012

Glucocorticoids - New Recognition of Our Familiar Friend

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“…Similar to immune cells, studies have suggested that fibroblasts might utilize TLRs for sense pathogens, resulting in the production of many mediators contributing to the control of the infection [8,9]. Gingival fibroblasts constitutively express TLR2, TLR3, and TLR4 [10], and also the adhesion molecules ICAM-1 (CD54) and CD44 [11,12]. Activation of gingival fibroblast with microbial products induced the production of proinflammatory cytokines [13,14].…”

Section: Introductionmentioning

confidence: 99%

Recognition of Candida albicans by gingival fibroblasts: The role of TLR2, TLR4/CD14, and MyD88

et al. 2018

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Recent evidence indicates that nonprofessional immune cells such as epithelial cells, endothelial cells, and fibroblasts also contribute to innate immunity via secretion of cytokines. Fibroblasts are the principal type of cell found in the periodontal connective tissues and they are involved in the immune response during periodontal disease. The role of fibroblasts in the recognition of pathogens via Toll-like receptors (TLRs) has been established; however, few studies have been conducted concerning the involvement of innate immune receptors in the recognition of Candida albicans by gingival fibroblast. In the current study, we investigate the functional activity of TLR2, cluster of differentiation 14 (CD14), and myeloid differentiation primary response gene 88 (MyD88) molecules in the recognition of C. albicans by gingival fibroblast. First, we identified that gingival fibroblasts expressed TLR2, TLR3, and TLR4. Our results showed that TLR agonists had no effect on these receptors’ expression by TLR2, MyD88, and CD14-deficient cells. Notably, C. albicans and a synthetic triacylated lipoprotein (Pam3CSK4) induced a remarkable increase of TLR3 expression on MyD88-deficient gingival fibroblasts. TLR4 expression levels were lower than TLR2 and TLR3 levels and remained unchanged after TLR agonist stimulation. Gingival fibroblasts presented morphological similarities; however, TLR2 deficiency on these cells leads to a lower proliferative response, whereas the deficiency on CD14 expression resulted in lower levels of type I collagen by these cells. In addition, the recognition of C. albicans by gingival fibroblasts had an effect on the secretion of cytokines and it was dependent on a specific recognition molecule. Specifically, tumor necrosis factor-α (TNF-α ) production after the recognition of C. albicans was dependent on MyD88, CD14, and TLR2 molecules, whereas the production of interleukin-1β (IL-1β ) and IL-13 was dependent on TLR2. These findings are the first to describe a role of gingival fibroblast in the recognition of C. albicans and the pathways involved in this process. An understanding of these pathways may lead to alternative treatments for patients with periodontal disease.

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In vitro effect of glucocorticoids on nasal polyps

Cited by 4 publications

References 23 publications

Single nucleotide polymorphisms in TNF are associated with susceptibility to aspirin-exacerbated respiratory disease but not to cytokine levels: a study in Mexican mestizo population

Single nucleotide polymorphisms in TNF are associated with susceptibility to aspirin-exacerbated respiratory disease but not to cytokine levels: a study in Mexican mestizo population

Glucocorticoid Resistance in the Upper Respiratory Airways

Recognition of Candida albicans by gingival fibroblasts: The role of TLR2, TLR4/CD14, and MyD88

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