Project description:Chronic rhinosinusitis is classified into eosinophilic chronic rhinosinusitis (ECRS) and non-eosinophilic chronic rhinosinusitis (NECRS). ECRS is a refractory allergic disease involving a variety of immune and epithelial cells. S100A8 is a damage-associated molecular pattern that is closely related to allergic inflammation. However, the pathological implications of S100A8 in ECRS have not been clarified. We evaluated the role of S100A8 in the pathogenesis of ECRS. Gene expression profiles of nasal polyps obtained from patients with ECRS or NECRS were evaluated using RNA sequencing. S100A8 was identified as a significantly upregulated gene in nasal polyps associated with ECRS. Consistently, immunohistochemistry revealed that S100A8 stained intensely in nasal polyps from patients with ECRS. Human nasal epithelial cells expressed the receptor for advanced glycation end products and Toll-like receptor 4. Recombinant S100A8 protein induced interleukin-1β secretion in human nasal epithelial cells. Our data demonstrate that S100A8 induces production of interleukin-1β in the nasal epithelium, which may be involved in the pathogenesis of ECRS.
Project description:Chronic rhinosinusitis with nasal polyps is a hallmaerk disease in the field of upper airway immunity and chronic inflammation. Diverse inflammatory patterns between nasal polyps have been described in patients that hail from disparate racial and geographic backgrounds. However, it remains unclear whether these immunologic differences in nasal polyps between racial groups are driven by unique molecular mechanisms. We interrogated the gene expression profiles of nasal polyp tissues from Western (United States) and East Asian (Japan) descent, compared to ethmoid sinus tissue controls.
Project description:Chronic rhinosinusitis with nasal polyps is a hallmaerk disease in the field of upper airway immunity and chronic inflammation. Diverse inflammatory patterns between nasal polyps have been described in patients that hail from disparate racial and geographic backgrounds. However, it remains unclear whether these immunologic differences in nasal polyps between racial groups are driven by unique molecular mechanisms. We interrogated the gene expression profiles of nasal polyp tissues from Western (United States) and East Asian (Japan) descent, compared to ethmoid sinus tissue controls.
Project description:Asthmatic chronic rhinosinusitis with nasal polyps (aCRSwNP) is a common disruptive eosinophilic disease. Therefore, we sought to identify gene expression changes in nasosinus inflamed mucosa and adjacent polyp tissue from subjects with aCRSwNP. Twelve asthmatic chronic rhinosinusitis (aCRS) subjects (11 with nasal polyps; aCRSwNP) provided inflamed nasosinus mucosa (11 samples) and adjacent polyp (10 samples) or a small mixed mucosa and polyp specimen (1 sample) (thus, 22 samples overall). Inflamed mucosa or polyp was from the middle meatus or anterior ethmoid cavity. As control samples, nasosinus tissue was collected from the inferior turbinate or uncinate process from normal or rhinitis subjects without nasal polyps (n=17); 4 had physician-diagnosed allergic rhinitis (AR), 2 had suspected AR, 1 had suspected vasomotor rhinitis, and 10 had no signs of nasosinus disease, allergy, or atopy. All 4 AR subjects chose to donate tissue outside of their known allergy season(s).
Project description:The pathways underlying chronic rhinosinusitis with nasal polyps (CRSwNP) are unclear. We conducted genome-wide gene expression analysis to determine pathways and candidate gene sets associated with CRSwNP.
Project description:Asthmatic chronic rhinosinusitis with nasal polyps (aCRSwNP) is a common disruptive eosinophilic disease. Therefore, we sought to identify gene expression changes in nasosinus inflamed mucosa and adjacent polyp tissue from subjects with aCRSwNP.
Project description:NSAID-exacerbated respiratory disease (N-ERD) represents a particularly severe endotype of chronic rhinosinusitis with nasal polyps (CRSwNP), which affects around 10-16% of CRSwNP patients. N-ERD is characterized by severe and refractory nasal polyposis, bronchial asthma and intolerance to non-steroidal anti-inflammatory drugs (NSAIDs), including aspirin. Today, the pathogenesis of N-ERD remains incompletely understood and curative treatments are lacking. Using a global transcriptomic approach, we identified local changes between the mucosa of N-ERD nasal polyps and healthy control inferior turbinates. Nasal brushing samples were collected from inferior turbinates of healthy controls and nasal polyps of N-ERD patients under anterior rhinoscopy and stored at -80°C in RNAprotect until RNA isolation and RNAseq.
Project description:Patients with chronic rhinosinusitis (CRS) have abnormal immune responses triggered by a variety of infectious agents, airborne toxins and fungi. Respiratory epithelial cells serve as relay stations capable of amplifying or augmenting cues received from external stimuli to nearby immune cells located in the sinus mucosa. Previous studies have identified increases in complement components and complement gene expression in the mucosa of patients with atopic CRS with nasal polyps (CRSwNP). As part of a larger study, we used shotgun proteomics to quantify changes in mucus proteins between patients with and without nasal polyps.
