Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0149514 (bronchitis)
 6,902 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pulmonary tuberculosis, one of the granulomatous diseases, has few serological markers for its activity. Recently, an increased serum level of vascular endothelial growth factor (VEGF) was detected in patients with Crohn's disease, also a granulomatous disease. We hypothesized that VEGF might be associated with the pathogenesis of pulmonary tuberculosis. We investigated the serum level of VEGF in 43 patients with active pulmonary tuberculosis, 29 patients with old tuberculosis, and 25 patients with acute bronchitis. We were able to examine the serum VEGF levels every 3 mo for a period of 6 mo in seven patients with active pulmonary tuberculosis. We examined the presence of VEGF in the resected lungs of three patients with active pulmonary tuberculosis by immunohistochemistry. The serum levels of VEGF were significantly higher in patients with active pulmonary tuberculosis than in patients with old tuberculosis and acute bronchitis. The decrease in titer of serum VEGF paralleled the clinical improvement of patients with pulmonary tuberculosis. Immunohistochemical staining of the resected lungs demonstrated the presence of VEGF in alveolar macrophages surrounding the lesion. Therefore, VEGF may be associated with the pathogenesis of pulmonary tuberculosis.
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PMID:Increased serum level of vascular endothelial growth factor in pulmonary tuberculosis. 1098 40

Asthma and eosinophilic bronchitis are characterized by a similar type of eosinophilic inflammation. However, eosinophilic bronchitis differs from asthma in that there is no variable airflow obstruction or airway hyperresponsiveness. We evaluated the roles of vascular endothelial growth factor (VEGF) and microvascular permeability in causing these differences between the two diseases. Inflammatory indexes in induced sputum, exhaled nitric oxide levels, and vascular permeability index were examined in 11 normal control subjects, 19 beclomethasone dipropionate (BDP)-treated subjects with asthma, 20 non-BDP-treated subjects with asthma, and 17 patients with eosinophilic bronchitis. The percentage of eosinophils in sputum and exhaled nitric oxide levels were significantly higher in non-BDP-treated subjects with asthma and patients with eosinophilic bronchitis than in other two groups; however, VEGF levels and vascular permeability index were significantly higher in non-BDP-treated (VEGF: mean; 4,710 [SD; 1,150] pg/ml, p < 0.0001; vascular permeability index: 0.028 [0.009], p < 0.0001) and BDP-treated (2,560 [1,070] pg/ml, p = 0.0002; 0.016 [0.006], p = 0.004) subjects with asthma than in patients with eosinophilic bronchitis (1,120 [800] pg/ml; 0.01 [0.005]) and normal control subjects (1,390 [1,280] pg/ml; 0.008 [0.003]). We found significant correlations between the VEGF level and the airway vascular permeability index in all patient groups. Thus, interaction between airway microcirculation and VEGF may be a key element in differences in airway function between asthma and eosinophilic bronchitis.
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PMID:Role of microvascular permeability on physiologic differences in asthma and eosinophilic bronchitis. 1522 Jan 18

ABSTARCT Epidemiological and clinical studies have increasingly shown that fine particulate matter (PM2.5) is associated with a number of pathological respiratory diseases, such as bronchitis, asthma, and chronic obstructive pulmonary disease, which share the common feature of airway inflammation induced by particle exposure. Thus, understanding how PM2.5 triggers inflammatory responses in the respiratory system is crucial for the study of PM2.5 toxicity. In the current study, we found that exposing human bronchial epithelial cells (immortalized Beas-2B cells and primary cells) to PM2.5 collected in the winter in Wuhan, a city in southern China, induced a significant upregulation of VEGFA (vascular endothelial growth factor A) production, a signaling event that typically functions to control chronic airway inflammation and vascular remodeling. Further investigations showed that macroautophagy/autophagy was induced upon PM2.5 exposure and then mediated VEGFA upregulation by activating the SRC (SRC proto-oncogene, non-receptor tyrosine kinase)-STAT3 (signal transducer and activator of transcription 3) pathway in bronchial epithelial cells. By exploring the upstream signaling events responsible for autophagy induction, we revealed a requirement for TP53 (tumor protein p53) activation and the expression of its downstream target DRAM1 (DNA damage regulated autophagy modulator 1) for the induction of autophagy. These results thus extend the role of TP53-DRAM1-dependent autophagy beyond cell fate determination under genotoxic stress and to the control of proinflammatory cytokine production. Moreover, PM2.5 exposure strongly induced the activation of the ATR (ATR serine/threonine kinase)-CHEK1/CHK1 (checkpoint kinase 1) axis, which subsequently triggered TP53-dependent autophagy and VEGFA production in Beas-2B cells. Therefore, these findings suggest a novel link between processes regulating genomic integrity and airway inflammation via autophagy induction in bronchial epithelial cells under PM2.5 exposure.
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PMID:TP53-dependent autophagy links the ATR-CHEK1 axis activation to proinflammatory VEGFA production in human bronchial epithelial cells exposed to fine particulate matter (PM2.5). 2746 84

Tussilagone (TSL) is a sesquiterpenoid isolated from Tussilago farfara, which has been used as a traditional medicine for the treatment of asthma and bronchitis. It also takes part in the anti-inflammatory and antioxidant effects, but its role in angiogenesis is unknown. Angiogenesis is a cancer feature that is essential for supplying oxygen and nutrients to all proliferating tumor cells. Here, we demonstrated that TSL significantly inhibited the proliferation, migration, invasion, and tube formation of primary human umbilical vascular endothelial cell (HUVEC) in vitro. Also, TSL inhibited vascular endothelial growth factor (VEGF)-induced angiogenesis revealed by Matrigel plug assay in vivo. At present, we observed that TSL inhibited the activity of VEGFR2 signal pathway induced by VEGF. These findings suggested that TSL may serve as a potential therapeutic target in the angiogenesis.
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PMID:Tussilagone Suppresses Angiogenesis by Inhibiting the VEGFR2 Signaling Pathway. 3133 73