bromochloroacetic-acid and Rhinitis

bromochloroacetic-acid has been researched along with Rhinitis* in 2 studies

Other Studies

2 other study(ies) available for bromochloroacetic-acid and Rhinitis

ArticleYear
Features of mesenchymal transition in the airway epithelium from chronic rhinosinusitis.
    Allergy, 2014, Volume: 69, Issue:11

    Chronic rhinosinusitis (CRS) defines a group of disorders characterized by persistent inflammation of the sinonasal tract. Epithelial changes and structural remodelling are present, but whether epithelial differentiation is altered remains uncertain.. To evaluate the differentiation state of the sinonasal epithelium in CRS, sinonasal biopsies from patients with CRS with nasal polyps (CRSwNP) or CRS without nasal polyps (CRSsNP), or with allergic rhinitis (AR), as compared to controls, were processed by immunohistochemistry and RT-qPCR for terminal differentiation (E-cadherin, high molecular weight cytokeratins (Hmw CK) and CK5, vimentin) and lineage differentiation (ß-tubulin IV+ ciliated cells, MUC5AC+ goblet cells, p63 + basal cells). Findings were correlated with subepithelial fibrosis and clinical CT score.. Expression of E-cadherin was decreased at protein and mRNA levels in CRSwNP and CRSsNP, as compared to controls. Staining for Hmw CKs was also reduced in CRSwNP and CRSsNP, and CK5 mRNA was decreased in CRSwNP. These features were not due to changes in lineage specification, but associated with increases in vimentin-expressing epithelial cells. In addition, vimentin expression correlated with the basement membrane thickening and with CT score, as well as with tissue eosinophils.. Features of epithelial dedifferentiation towards a mesenchymal phenotype are observed in CRSwNP and CRSsNP and correlate with airway fibrosis and inflammation.

    Topics: Adolescent; Adult; Aged; Airway Remodeling; Cadherins; Case-Control Studies; Cell Count; Cell Dedifferentiation; Chronic Disease; Epithelial-Mesenchymal Transition; Female; Fibrosis; Gene Expression; Goblet Cells; Humans; Keratins; Male; Middle Aged; Nasal Polyps; Phenotype; Respiratory Mucosa; Rhinitis; Risk Factors; Sinusitis; Tomography, X-Ray Computed; Vimentin; Young Adult

2014
GM-CSF, IL-8, IL-1R, TNF-alpha R, and HLA-DR in nasal epithelial cells in allergic rhinitis.
    American journal of respiratory and critical care medicine, 1996, Volume: 153, Issue:5

    Epithelial cells potentially contribute to airways inflammation by antigen presentation and the production of proinflammatory cytokines. This study investigated the immunocytochemical localization of interleukin-8 (IL-8), granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin-1 receptor (IL-1R Type I), tumor necrosis factor-alpha receptor (TNF-alpha R; 55kD), and human leukocyte antigen-DR (HLA-DR) on epithelial cells obtained by nasal brushing from 10 patients with allergic rhinitis in season and 15 healthy, nonallergic subjects. Six of the 15 nonallergic asymptomatic subjects had macroscopic evidence of nasal mucosal inflammation, and their brushings contained more than 10% neutrophils ("subclinical inflammation"). In normal control subjects, 8 +/- 7.5% of epithelial cells stained for HLA-DR, approximately one quarter stained for IL-8 and GM-CSF, and about one third stained positive for IL-1R and TNF-alpha R. The findings in subjects with allergic rhinitis in season and with subclinical neutrophilia were similar, and the numbers of cells staining for HLA-DR expression correlated with both neutrophil and lymphocyte content. These findings further support the conclusion that epithelial cells can contribute to inflammatory processes in the nasal mucosa. The findings emphasize the need to identify asymptomatic nasal mucosal inflammation in studies of the nasal mucosa.

    Topics: Adolescent; Adult; Eosinophils; Epithelium; Granulocyte-Macrophage Colony-Stimulating Factor; HLA-DR Antigens; Humans; Interleukin-8; Keratins; Leukocyte Count; Macrophages; Middle Aged; Nasal Mucosa; Neutrophils; Receptors, Interleukin-1; Receptors, Tumor Necrosis Factor; Rhinitis; Rhinitis, Allergic, Seasonal; T-Lymphocytes, Helper-Inducer; Tumor Necrosis Factor-alpha

1996