Although histologic features of airway remodeling have been well characterized in asthma, the immunologic and inflammatory mechanisms that drive progression of asthma to remodeling are still incompletely understood. Conceptually, airway remodeling may be a result of persistent inflammation and/or aberrant tissue repair mechanisms. It is likely that several immune and inflammatory cell types and mediators are involved in mediating airway remodeling. In addition, different features of airway remodeling are likely mediated by different inflammatory pathways. Several important candidate mediators of remodeling have been identified, including TGF-beta and T(H)2 cytokines (including IL-5 and IL-13), as well as vascular endothelial growth factor, a disintegrin and metalloproteinase 33, and matrix metalloproteinase 9. Mouse models of airway remodeling have provided important insight into potential mechanisms by which TGF-beta activation of the Smad-2/3 signaling pathway may contribute to airway remodeling. Human studies have demonstrated that anti-IL-5 reduces levels of airway eosinophils expressing TGF-beta, as well as levels of airway remodeling as assessed by bronchial biopsies. Further such studies confirming these observations, as...Continue Reading
Effects of treatment on airway inflammation and thickening of basement membrane reticular collagen in asthma. A quantitative light and electron microscopic study
Transforming growth factor beta 1 (TGF beta 1) gene expression by eosinophils in asthmatic airway inflammation
Effect of short-term treatment with low-dose inhaled fluticasone propionate on airway inflammation and remodeling in mild asthma: a placebo-controlled study
Increased release of matrix metalloproteinase-9 in bronchoalveolar lavage fluid and by alveolar macrophages of asthmatics
Collagen deposition in large airways may not differentiate severe asthma from milder forms of the disease
Pulmonary expression of interleukin-13 causes inflammation, mucus hypersecretion, subepithelial fibrosis, physiologic abnormalities, and eotaxin production
Inhaled corticosteroids decrease subepithelial collagen deposition by modulation of the balance between matrix metalloproteinase-9 and tissue inhibitor of metalloproteinase-1 expression in asthma
Relation of CD4+CD25+ regulatory T-cell suppression of allergen-driven T-cell activation to atopic status and expression of allergic disease
Defective suppression of Th2 cytokines by CD4CD25 regulatory T cells in birch allergics during birch pollen season
Vascular endothelial growth factor (VEGF) induces remodeling and enhances TH2-mediated sensitization and inflammation in the lung
Mouse Siglec-F and human Siglec-8 are functionally convergent paralogs that are selectively expressed on eosinophils and recognize 6'-sulfo-sialyl Lewis X as a preferred glycan ligand
Acute and chronic airway responses to viral infection: implications for asthma and chronic obstructive pulmonary disease
Animal models of allergen-induced tolerance in asthma: are T-regulatory-1 cells (Tr-1) the solution for T-helper-2 cells (Th-2) in asthma?
Interleukin 25 regulates type 2 cytokine-dependent immunity and limits chronic inflammation in the gastrointestinal tract.
Bradykinin-induced asthmatic fibroblast/myofibroblast activities via bradykinin B2 receptor and different MAPK pathways
Correlation of hyaluronan deposition with infiltration of eosinophils and lymphocytes in a cockroach-induced murine model of asthma.
CD4+CD25-mTGFbeta+ T cells induced by nasal application of ovalbumin transfer tolerance in a therapeutic model of asthma
Comparative microarray analysis and pulmonary changes in Brown Norway rats exposed to ovalbumin and concentrated air particulates
PI3K gamma-deficient mice have reduced levels of allergen-induced eosinophilic inflammation and airway remodeling.
Allergen-induced coexpression of bFGF and TGF-β1 by macrophages in a mouse model of airway remodeling: bFGF induces macrophage TGF-β1 expression in vitro
Inhibiting AKT phosphorylation employing non-cytotoxic anthraquinones ameliorates TH2 mediated allergic airways disease and rhinovirus exacerbation
Antileukotriene reverts the early effects of inflammatory response of distal parenchyma in experimental chronic allergic inflammation
Protein and microRNA biomarkers from lavage, urine, and serum in military personnel evaluated for dyspnea
Inhibitory effects of anti-immunoglobulin E antibodies on airway remodeling in a murine model of chronic asthma
The effects of antisense interleukin-4 gene transferred by recombinant adeno-associated virus vector on the airway remodeling in allergic rats
Functional Effects of WNT1-Inducible Signaling Pathway Protein-1 on Bronchial Smooth Muscle Cell Migration and Proliferation in OVA-Induced Airway Remodeling
Immunization against TGF-β1 reduces collagen deposition but increases sustained inflammation in a murine asthma model
Airway Remodeling in Chronic Obstructive Pulmonary Disease and Asthma: the Role of Matrix Metalloproteinase-9
Epoxyeicosatrienoic acids are involved in the C(70) fullerene derivative-induced control of allergic asthma.
Human matrix metalloproteinases: an ubiquitarian class of enzymes involved in several pathological processes
Systemic and exhaled cytokine and chemokine profiles are associated with the development of bronchiolitis obliterans syndrome
Inhalation exposure to sulfur mustard in the guinea pig model: clinical, biochemical and histopathological characterization of respiratory injuries
Severe Persistent Allergic Rhinitis. Inflammation but No Histologic Features of Structural Upper Airway Remodeling
Allergy and Asthma
Allergy and asthma are inflammatory disorders that are triggered by the activation of an allergen-specific regulatory t cell. These t cells become activated when allergens are recognized by allergen-presenting cells. Here is the latest research on allergy and asthma.
Arterial-Venous in Development & Disease
Arterial-venous development may play a crucial role in cardiovascular diseases. Here is the latest research.
This feed focuses in Asthma in which your airways narrow and swell. This can make breathing difficult and trigger coughing, wheezing and shortness of breath.