OSM levels in lysates of nasal polyps and uncinate tissue positively correlated with levels of α2-macroglobulin, a marker of epithelial leak, in localized nasal secretions (r = 0.4855, P < .05).
Institutional review board-approved study examining mucus concentrations of P-gp in 36 patients (10 control, 16 CRS without nasal polyps [CRSsNP], and 10 CRS with nasal polyps [CRSwNP]).
Recent studies have associated osteitis with nasal polyps and tissue eosinophilia with the increase in periostin expression and P-glycoprotein mucosal expression.
ACT-774312 is an antagonist of the chemoattractant receptor-homologous molecule expressed on T helper (Th) 2 cells (CRTH2), in development for the treatment of nasal polyposis or other allergic and type-2 inflammatory diseases.
ACT-774312 is an antagonist of the chemoattractant receptor-homologous molecule expressed on T helper (Th) 2 cells (CRTH2), in development for the treatment of nasal polyposis or other allergic and type-2 inflammatory diseases.
ACT-774312 is an antagonist of the chemoattractant receptor-homologous molecule expressed on T helper (Th) 2 cells (CRTH2), in development for the treatment of nasal polyposis or other allergic and type-2 inflammatory diseases.
ACT-774312 is an antagonist of the chemoattractant receptor-homologous molecule expressed on T helper (Th) 2 cells (CRTH2), in development for the treatment of nasal polyposis or other allergic and type-2 inflammatory diseases.
ADAM-33 staining was increased in the mesenchymal cells of vessels of nasal polyps (median, 2; range, 1-3) compared with control tissues (median, 1.5; range, 1-2; p = 0.006).
The observed associations between the ADRB2 argl6gly polymorphism and asthma-related phenotypes as well as those between nasal polyposis and asthma have prompted us to evaluate the potential involvement of this polymorphism in sinonasal polyposis.
High motility group box 1 (HMGB1) protein and its receptor for advanced glycation end products (RAGE) expression in chronic rhinosinusitis without nasal polyps.
The mRNA expression levels of miRNA machinery components including Drosha, Dicer, protein activator of the interferon-induced protein kinase (PACT), human immunodeficiency virus transactivating response RNA-binding protein, fragile X mental retardation protein, and argonaute 2/eukaryotic translation initiation factor 2C, 2 in nasal biopsies from control, CRS without nasal polyps (CRSsNP), eosinophilic, and noneosinophilic CRS with nasal polyps (CRSwNP) subjects were determined by quantitative reverse transcription polymerase chain reaction.
The aim of the present study was to investigate whether AhR, which regulates Th17 cell differentiation, played a role in the pathogenesis of CRSwNP by evaluating AhR expression in nasal polyps and peripheral blood mononuclear cells (PBMCs) obtained from CRSwNP patients.
In a murine nasal polyp (NP) model, blocking the p38 and ERK signaling pathways prevented NP formation and chemotactic cytokine secretion by neutrophils but not eosinophils.
Expression levels of 16 genes were found to be modulated in polyps including AID, IgG and IgE mature transcripts which reflect AID activity; clustering algorithm revealed an AID-specific gene signature for the disease state with nasal polyp.
In a murine nasal polyp (NP) model, blocking the p38 and ERK signaling pathways prevented NP formation and chemotactic cytokine secretion by neutrophils but not eosinophils.