Smith TL, Kern R, Palmer JN, et al. population, various treatment options, and exhaled nitric oxide are briefly addressed. biofilm-associated CRS, the relative contributions of staphylococcal superantigens, and biofilms in the inflammatory makeup of this disease has been documented.7 biofilms are associated with eosinophilic inflammation, across the spectrum of CRS, on the back Perifosine (NSC-639966) of a Th2 skewing of the host’s adaptive immune response, elevated eosinophilic cationic protein, and IL-5.7 Bacterial biofilms in CRS, biofilms, and exotoxins that act as superantigens have been implicated in playing an important pathological role in the incidence, maintenance, and ongoing burden of CRS.8 A better understanding of the interplay between bacterial factors, host factors, and the environment will facilitate better management of this disease.8 Adaptive humoral immune responses in the airways are mediated by B cells and plasma cells that express highly evolved and specific receptors and produce immunoglobulins of most isotypes. A recent review discussed the generation, differentiation, signaling, activation, and recruitment pathways of B cells and plasma cells, with special emphasis on unique characteristics of subsets of these cells functioning within the respiratory system.9 Antigen exposure in the upper or lower airways can also drive expansion of B-lineage cells in the airway mucosal tissue and lead to the formation of inducible lymphoid follicles or aggregates that can mediate local immunity or disease.9 REMODELING IN ASTHMA AND CHRONIC SINUSITIS Asthma pathophysiology involves airway inflammation, epithelial, smooth muscle dysfunction, and airway remodeling.10 Airway remodeling includes cellular proliferation, increased matrix protein deposition, basement membrane thickening, and angiogenesis.11 Alveolar epithelial cells may be more important in remodeling than bronchial epithelial Perifosine (NSC-639966) cells. Vascular endothelia growth factor (VEGF) secretion from allergen-stimulated alveolar epithelial cells and expression of cell-associated VEGF was shown.12 is a common inhalant, indoor allergen, known for causing AR and airway inflammation. VEGF secretions from normal human lung fibroblasts and a dose-dependent fashion was shown to increase aggregation of human lung microvascular endothelial cells in response to transforming growth factor (TGF) , in conditioned media from (Der p1) with confluent alveolar epithelial cells.13 Detection of airway remodeling in subsets of asthma is difficult and clinically useful biomarkers are needed. A selected panel of cytokines, growth factors, fractional exhaled nitric oxide (FeNO), and possible radiographic imaging may assist clinicians in detecting and providing targeting therapy.14 A defect in barrier function and an impaired innate immune response to viral infection may provide the substrate on which allergic sensitization occurs. The repeated allergen exposure will lead to disease persistence that could also be used to explain airway wall remodeling and the susceptibility of the asthmatic lung to exacerbations.14 Asthma progression may be caused by persistent airway inflammation and/or impaired repair mechanisms. Allergen inhalation induces activation of Th2 cells, which express cytokines including IL-5, which generates TGF-+ eosinophils that promote features of remodeling. Chronic asthma is characterized by enhanced epithelialCmesenchymal communications with the release of a range of different growth factors linked to remodeling.15 The relative sensitivities of two markers of proliferation, proliferating cell nuclear antigen, and Ki-67, in airway smooth muscle, from subjects with moderate or severe asthma and healthy controls and was evaluated whether muscle remodeling is a dynamic process in asthma by quantifying the proliferation rate.16 Proliferating cell nuclear antigen was a highly sensitive marker of proliferation and heparin-binding epidermal growth factor was noted to be a potential biomarker during active remodeling of airway smooth muscle in severe asthma.16 Phenotypes of CRS can be differentiated based on mucosal remodeling and inflammatory patterns.17 CRS can be differentiated into several subgroups based on specific remodeling, inflammatory cell, and cytokine patterns.17 Current knowledge of factors that may predict asthma comorbidity in patients with CRS has confirmed that the same factors are also associated with severe asthma.17 TGF-?1 is a major participant in the airway remodeling of asthma, and enhanced epithelial immunoreactivity is known to occur in AR.18 allergens from dialyzed standardized immunotherapy extract was shown to induce apoptosis and increase. National Asthma Education and Prevention Program. airway, genetics, an integral part in asthma, and CRS. TNF In addition, the role of vitamin D in both asthma and CRS in the elderly and pediatric population, various treatment options, and exhaled nitric oxide are briefly addressed. biofilm-associated CRS, the relative contributions of staphylococcal superantigens, and biofilms in the inflammatory makeup of this disease has been documented.7 biofilms are associated with eosinophilic inflammation, across the spectrum of CRS, on the back of a Th2 skewing of the host’s adaptive immune response, elevated eosinophilic cationic protein, and IL-5.7 Bacterial biofilms in CRS, biofilms, and exotoxins that act as superantigens have been implicated in playing an important pathological role in the incidence, maintenance, and ongoing burden of CRS.8 A better understanding of the interplay between bacterial factors, host factors, and the environment will facilitate better management of this disease.8 Adaptive humoral immune responses in the airways are mediated by B cells and plasma cells that express highly evolved and specific receptors and produce immunoglobulins of most isotypes. A recent review discussed the generation, differentiation, signaling, activation, and recruitment pathways of B cells and plasma cells, with special Perifosine (NSC-639966) emphasis on unique characteristics of subsets of these cells functioning within the respiratory system.9 Antigen exposure in the upper or lower airways can also drive expansion of B-lineage cells in the airway mucosal tissue and lead to the formation of inducible lymphoid follicles or aggregates that can mediate local immunity or disease.9 REMODELING IN ASTHMA AND CHRONIC SINUSITIS Asthma pathophysiology involves airway inflammation, epithelial, smooth muscle dysfunction, and airway remodeling.10 Airway remodeling includes cellular proliferation, increased matrix protein deposition, basement membrane thickening, and angiogenesis.11 Alveolar epithelial cells may be more Perifosine (NSC-639966) important in remodeling than bronchial epithelial cells. Vascular endothelia growth factor (VEGF) secretion from allergen-stimulated alveolar epithelial cells and expression of cell-associated VEGF was shown.12 is a common inhalant, indoor allergen, known for causing AR and airway inflammation. VEGF secretions from normal human lung fibroblasts and a dose-dependent fashion was shown to increase aggregation of human lung microvascular endothelial cells in response to transforming growth factor (TGF) , in conditioned media from (Der p1) with confluent alveolar epithelial cells.13 Detection of airway remodeling in subsets of asthma is difficult and clinically useful biomarkers are needed. A selected panel of cytokines, growth factors, fractional exhaled nitric oxide (FeNO), and possible radiographic imaging may assist clinicians in detecting and providing targeting therapy.14 A defect in barrier function and an impaired innate immune response to viral infection may provide the substrate on which allergic sensitization occurs. The repeated allergen exposure will lead to disease persistence that could also be used to explain airway wall remodeling and the susceptibility of the asthmatic lung to exacerbations.14 Asthma progression may be caused by persistent airway inflammation and/or impaired repair mechanisms. Allergen inhalation induces activation of Th2 cells, which express cytokines including IL-5, which generates TGF-+ eosinophils that promote features of remodeling. Chronic asthma is characterized by enhanced epithelialCmesenchymal communications with the release of a range of different growth factors linked to remodeling.15 The relative sensitivities of two markers of proliferation, proliferating cell nuclear antigen, and Ki-67, in airway smooth muscle, from subjects with moderate or severe asthma and healthy controls and was evaluated whether muscle remodeling is a dynamic process in asthma by quantifying the proliferation rate.16 Proliferating cell nuclear antigen was a highly sensitive marker of proliferation and heparin-binding epidermal growth factor was noted to be a potential biomarker during active remodeling of airway smooth muscle in severe asthma.16 Phenotypes of CRS can be differentiated based on mucosal remodeling and inflammatory patterns.17 CRS can be differentiated into several subgroups based on specific remodeling, inflammatory cell, and cytokine patterns.17 Current knowledge of factors that may predict asthma comorbidity in patients with CRS has confirmed that the same factors are also associated with severe asthma.17 TGF-?1 is a major participant in the airway remodeling of asthma, and enhanced epithelial immunoreactivity is known to occur in AR.18 allergens from dialyzed standardized immunotherapy extract was shown to induce apoptosis and increase TGF-?1 secretion in confluent A549 cells treated.