Silver nanoparticles modify VEGF signaling pathway and mucus hypersecretion in allergic airway inflammation

The anti-inflammatory action of silver nanoparticles (NPs) has been reported in a murine model of asthma in a previous study. But more specific mechanisms of silver NPs in an attenuation of allergic airway inflammation have not yet been established. Vascular and mucous changes are believed to contribute largely in pathophysiology in asthma. Among various factors related to vascular changes, vascular endothelial growth factor (VEGF) plays a pivotal role in vascular changes in asthma. Mucin proteins MUC5AC and MUC5B have been implicated as markers of goblet cell metaplasia in lung pathologies. The aim of this study was to investigate the effects of silver NPs on VEGF signaling pathways and mucus hypersecretion. Ovalbumin (OVA)-inhaled female BALBc mice were used to evaluate the role of silver NPs and the related molecular mechanisms in allergic airway disease. In this study, with an OVA-induced murine model of allergic airway disease, it was found that the increased levels of hypoxia-inducible factor (HIF)-1α, VEGF, phosphatidylinositol-3 kinase (PI3K) and phosphorylated-Akt levels, and mucous glycoprotein expression (Muc5ac) in lung tissues were substantially decreased by the administration of silver NPs. In summary, silver NPs substantially suppressed mucus hypersecretion and PI3K/HIF-1α/VEGF signaling pathway in an allergic airway inflammation

A Case of Granular Cell Tumor of the Trachea

A 20-year-old man presented to our outpatient clinic with hemoptysis, cough, and pleuritic chest pain. His chest radiograph and pulmonary function tests (PFT) were normal. A bronchoscopy showed a small yellowish patch with a regular surface. A direct bronchoscopic biopsy was performed. The pathologic findings showed a benign granular cell tumor. The respiratory symptoms resolved after biopsying the tumor. On follow.up, there were no signs of recurrence of the granular cell tumor after a period of 24 months

Screening of Brain Metastasis with Limited Magnetic Resonance Imaging (MRI): Clinical Implications of Using Limited Brain MRI During Initial Staging for Non-small Cell Lung Cancer Patients

The purpose of this prospective study was to determine whether using magnetic resonance imaging (MRI) for early screening for brain metastases (BM) can improve quality of life, survival in patients with non-small cell lung cancer (NSCLC). The study group comprised 183 patients newly diagnosed with NSCLC. All patients underwent limited brain MRI and routine workups. The control group comprised 131 patients with NSCLC who underwent limited brain MRI only if they had neurologic symptoms. The incidence of BM was 20.8% (38/183) in the study group and 4.6% (6/131) in the control group. The rate of upstaging based on the MRI data was 13.5% (15/111) overall and 15.9% (11/69) in patients that had been considered initially to be resectable surgically. There was no significant difference in survival outcome between the groups. Patients who had BM alone had a greater overall survival time (49 weeks) than those who had multiple systemic metastases (27 weeks; p=0.0307). In conclusions, limited brain MRI appears to be a useful, cost-effective method to screen for BM at the time of initial staging. And it may facilitate timely treatment of patients with NSCLC and improve their survival and quality of life

Pinus glabra - As a potential source of anti-Mycobacterium tuberculosis agent: Phytochemical and antimicrobial studies of its stem extracts

<p>(A) Numbers of patients with community acquired pneumonia and adenovirus pneumonia by week during January–May 2015. (B) Number of patients with adenovirus pneumonia (HAdV) and non-adenovirus pneumonia by military training week among newly recruited trainees (≤12 weeks of training or service period).</p

Inhibition of Lewis Lung Carcinoma Growth by Toxoplasma gondii through Induction of Th1 Immune Responses and Inhibition of Angiogenesis

Toxoplasma gondii is an obligate intracellular protozoan parasite that induces antitumor activity against certain types of cancers. However, little information is available regarding the immunologic mechanisms that regulate these effects. For this purpose, C57BL/6 mice were administered either the T. gondii Me49 strain orally or Lewis lung carcinoma (LLC) cells intramuscularly. Survival rates, tumor size, histopathology, and immune responses were determined for each group, and angiogenesis was evaluated by in vivo Matrigel plug assay. Toxoplasma-infected (TG-injected) mice survived the entire experimental period, whereas cancer cell-bearing (LLC-injected) mice died within six weeks. Mice injected with both T. gondii and cancer cells (TG/LLC-injected group) showed significantly increased survival rates, CD8+ T-cell percentages, IFN-γ mRNA expression levels, serum IgG2a titers, and CTL responses as compared to the LLC-injected mice. In addition, angiogenesis in the TG/LLC-injected mice was notably inhibited. These effects in TG/LCC-injected mice were similar or were increased by the addition of an adjuvant, Quil-A. However, TG/LLC-injected mice showed decreased percentages of CD4+ and CD8+ T-cells, IFN-γ mRNA expression levels, and serum IgG1 and IgG2a titers as compared to TG-injected mice. Taken together, our results demonstrate that T. gondii infection inhibits tumor growth in the Lewis lung carcinoma mouse model through the induction of Th1 immune responses and antiangiogenic activity

Reactive Oxygen Species Enhance TLR10 Expression in the Human Monocytic Cell Line THP-1

We investigated TLR10 expression in human monocytes, THP-1 cells, cultured in hypoxia (3% O2). Levels of both TLR10 mRNA and protein in THP-1 cells cultured in hypoxia were significantly higher than those cultured in normoxia (20% O2). We examined intracellular reactive oxygen species (ROS) content in hypoxic cells, and TLR10 expression in cells treated with hydrogen peroxide (H2O2), to determine whether the increase in TLR10 expression observed with hypoxia was due to an increase in intracellular ROS levels. We found that the level of intracellular ROS in cells subject to hypoxia was significantly higher than in normoxia. Experiments with ROS synthesis inhibitors revealed that hypoxia induced ROS production is mainly due to NADPH oxidase activity. TLR10 mRNA expression was increased by treatment with H2O2 at concentrations ranging from 50 to 250 μM. We screened the TLR10 promoter and found putative binding sites for transcription factors (TFs), such as NF-κB, NF-AT and AP-1. Next, we examined TF activities using a luciferase reporter assay. Activities of NF-κB, NF-AT and AP-1 in the cells treated with H2O2 were significantly higher than in untreated cells. The experiment with TF inhibitors revealed that ROS-induced upregulation of TLR10 expression is mainly due to NF-κB activation. Overall, our results suggest that hypoxia or ROS increase TLR10 expression in human monocytes and the transcriptional activities of NF-κB are involved in this process. Therefore, it is suggested that ROS produced by various exogenous stimuli may play a crucial role in the regulation of expression and function of TLR10 as second messengers