Chronic rhinosinusitis (CRS) is one of the most common chronic diseases and is associated with a high socioeconomic burden from direct and indirect costs. Its estimated prevalence ranges widely, from 2 to 16%. It is more common in female subjects, aged 18-64 years, and in southern and midwestern regions of the United States. CRS is more prevalent in patients with comorbid diseases such as asthma, chronic obstructive pulmonary disease, and environmental allergies. Few studies examine patient ethnicity, socioeconomic status, geographic location, and cultural factors in CRS populations. This article provides an overview of the epidemiology, racial variations, and economic burden of CRS.
Background-Obstructive sleep apnea (OSA) and central sleep apnea are common in patients with heart failure. We hypothesized that in such patients, severity of OSA is related to overnight rostral leg fluid displacement and increase in neck circumference, severity of central sleep apnea is related to overnight rostral fluid displacement and to sleep PCO 2 , and continuous positive airway pressure alleviates OSA in association with prevention of fluid accumulation in the neck. Methods and Results-In 57 patients with heart failure (ejection fraction Յ45%), we measured change in leg fluid volume and neck circumference before and after polysomnography, and we measured transcutaneous PCO 2 during polysomnography. Patients were divided into an obstructive-dominant group (Ն50% of apneas and hypopneas obstructive) and a central-dominant group (Ͼ50% of events central
Background-Epithelial barrier dysfunction is thought to play a role in many mucosal diseases including asthma, chronic rhinosinusitis (CRS), and eosinophilic esophagitis (EoE).
BackgroundChronic rhinosinusitis (CRS) with nasal polyps (CRSwNP) is characterized by type 2 inflammation with high levels of Th2 cytokines. Although T helper cytokines are released from T cells, innate lymphoid cells (ILC) are also known to produce high levels of the same cytokines. However, the presence of various types of ILC in CRS is poorly understood.ObjectiveThe objective of this study was to fully characterize the presence of all ILC subsets in CRS and to identify phenotypical differences of group 2 ILC (ILC2) in CRSwNP compared to ILC2 from non‐type 2 inflamed areas.MethodsWe investigated the presence of ILC subsets in peripheral blood mononuclear cells (PBMC) from healthy subjects, tonsil tissue, ethmoid tissue from control subjects and patients with non‐polypoid CRS (CRSsNP) and CRSwNP, as well as nasal polyp (NP) tissue from CRSwNP by flow cytometry. Sorted ILC2 were cultured in the presence and absence of IL‐33 and production of IL‐5 and IL‐13 was assessed by Luminex.ResultsWe found that all ILC subsets were present in NP but ILC2 were dominant and significantly elevated compared to PBMC, tonsil, CRSsNP, and normal sinus tissue. We also found that inducible T‐cell co‐stimulator (ICOS) and side scatter were increased and CD127 was down‐regulated in ILC2 from NP compared to blood or tonsil ILC2. Thymic stromal lymphopoietin, IL‐7, and IL‐33 were able to down‐regulate expression of CD127 and increase side scatter in blood ILC2. Furthermore, sorted NP ILC2 but not blood ILC2 spontaneously released type 2 cytokines including IL‐5 and IL‐13.Conclusions and Clinical RelevanceThese results suggest that ILC2 are not only elevated but also activated in CRSwNP in vivo and that ILC2 may play important roles in the type 2 inflammation in CRSwNP.
Background
We have previously shown that Oncostatin M (OSM) is elevated in nasal polyps of chronic rhinosinusitis (CRS) patients, as well as in bronchoalveolar lavage (BAL) fluids after segmental allergen challenge in allergic asthmatics. We also showed in vitro that physiological levels of OSM impair barrier function in differentiated airway epithelium.
Objective
We sought to determine which hematopoietic or resident cell type(s) were the source of the OSM expressed in mucosal airways disease.
Methods
Paraffin-embedded NP sections were stained with fluorescence-labeled specific antibodies against OSM, GM-CSF and hematopoietic cell specific markers. Live cells were isolated from NP and matched blood samples for flow cytometric analysis. Neutrophils were isolated from whole blood, cultured with the known OSM inducers GM-CSF and FSTL1, and levels of OSM were measured in the supernatants. Bronchial biopsy sections from controls, moderate asthmatics and severe asthmatics were stained for OSM and neutrophil elastase.
Results
OSM staining was observed in NP, showed co-localization with neutrophil elastase (n=10), and did not co-localize with markers for eosinophils, macrophages, T cells or B cells (n=3–5). Flow cytometric analysis of NP (n=9) showed that 5.1±2% of CD45+ cells were OSM+, and of the OSM+ cells, 56±7% were CD16+Siglec8−, indicating neutrophil lineage. Only.6±.4% of CD45+ events from matched blood samples (n=5) were OSM+, suggesting that elevated OSM in CRS was locally stimulated and produced. A majority of OSM+ neutrophils expressed Arginase 1 (72.5±12%), suggesting a N2 phenotype. GM-CSF was elevated in nasal polyp tissue compared to control, and was sufficient to induce OSM production (p<.001) in peripheral blood neutrophils in vitro. OSM+ neutrophils were also observed at elevated levels in biopsies from patients with severe asthma. Additionally, OSM protein was elevated in induced sputum from asthmatic patients compared to controls (p<.05).
Conclusions
Neutrophils are a major source of OSM producing cells in CRS and severe asthma.
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