epiglucan and Pulmonary-Eosinophilia

The biological and chemical natures of materials adsorbed onto fine particulate matter (PM2.5) vary by origin and passage routes. The exacerbating effects of the two samples-urban PM2.5 (U-PM2.5) collected during the hazy weather in a Chinese city and fine particles (ASD-PM2.5) collected during Asian sand dust (ASD) storm event days in Japan-on murine lung eosinophilia were compared to clarify the role of toxic materials in PM2.5. The amounts of β-glucan and mineral components were higher in ASD-PM2.5 than in U-PM2.5. On the other hand, organic chemicals, including polycyclic aromatic hydrocarbons (PAHs), were higher in U-PM2.5 than in ASD-PM2.5. When BALB/c mice were intratracheally instilled with U-PM2.5 and ASD-PM2.5 (total 0.4 mg/mouse) with or without ovalbumin (OVA), various biological effects were observed, including enhancement of eosinophil recruitment induced by OVA in the submucosa of the airway, goblet cell proliferation in the bronchial epithelium, synergic increase of OVA-induced eosinophil-relevant cytokines and a chemokine in bronchoalveolar lavage fluid, and increase of serum OVA-specific IgG1 and IgE. Data demonstrate that U-PM2.5 and ASD-PM2.5 induced allergic inflammatory changes and caused lung pathology. U-PM2.5 and ASD-PM2.5 increased F4/80(+) CD11b(+) cells, indicating that an influx of inflammatory and exudative macrophages in lung tissue had occurred. The ratio of CD206 positive F4/80(+) CD11b(+) cells (M2 macrophages) in lung tissue was higher in the OVA+ASD-PM2.5 treated mice than in the OVA+U-PM2.5 treated mice. These results suggest that the lung eosinophilia exacerbated by both PM2.5 is due to activation of a Th2-associated immune response along with induced M2 macrophages and the exacerbating effect is greater in microbial element (β-glucan)-rich ASD-PM2.5 than in organic chemical-rich U-PM2.5.

Topics: Air Pollutants; Allergens; Animals; beta-Glucans; Bronchoalveolar Lavage Fluid; Cell Count; China; Cytokines; Immunoglobulin E; Immunoglobulin G; Japan; Lung; Male; Metals; Mice, Inbred BALB C; Ovalbumin; Particulate Matter; Pulmonary Eosinophilia

Urban particulate matter (PM) is associated with an increase in asthma. PM2.5 (

Topics: Air Pollutants; Allergens; Animals; beta-Glucans; Bronchoalveolar Lavage Fluid; Cell Count; China; Cities; Cytokines; Heme Oxygenase-1; Immunoglobulin E; Immunoglobulin G; Lipopolysaccharides; Lung; Male; Membrane Proteins; Mice; Mice, Inbred BALB C; Nitric Oxide Synthase Type II; Ovalbumin; Particle Size; Particulate Matter; Pulmonary Eosinophilia; RAW 264.7 Cells; Respiratory Hypersensitivity

Our aim in the study was to investigate the pathogenesis of eosinophilic inflammation in patients with acute eosinophilic pneumonia (AEP), and to determine the levels of (1-->3)-beta-D-glucan, which is one of the major components of the cell wall of most fungi, in the BAL fluid (BALF) of those patients with AEP. Six patients with AEP and five patients with chronic eosinophilic pneumonia (CEP) that was in the acute stage and had been newly diagnosed, and nine healthy subjects from the Kurume University School of Medicine and the Social Institute Tagawa Hospital between 1995 and 2001 were entered into the study. In AEP patients, (1-->3)-beta-D-glucan was detected in BALF, and these findings were compared with BALF findings in patients with CEP as well as with those in healthy subjects. In the BALF of AEP patients, the mean concentration of (1-->3)-beta-D-glucan was significantly higher (p < 0.05) than that of CEP patients as well as healthy subjects. In patients with AEP, the mean concentration of (1-->3)-beta-D-glucan in BALF was significantly higher (p < 0.05) than that in the blood. In four of six patients with AEP, we measured serial changes in (1-->3)-beta-D-glucan levels, and the level of (1-->3)-beta-D-glucan in the BALF decreased with clinical improvement at follow-up. We concluded that inhaled (1-->3)-beta-D-glucan may be involved in the mechanisms of pulmonary inflammation in patients with AEP.

Topics: Acute Disease; Adolescent; Adult; Aged; Aged, 80 and over; beta-Glucans; Bronchoalveolar Lavage Fluid; Chronic Disease; DNA Fragmentation; DNA, Fungal; Female; Glucans; Humans; Male; Middle Aged; Pneumocystis; Pulmonary Eosinophilia

Moulds are present in a variety of environments and aerosols of fungal spores are generated when mouldy materials are handled. Molds contain (1-->3)-beta-D-glucan, a polyglucose which is present in the cell wall of fungi, certain bacteria and plants.. This study was undertaken to investigate the cellular inflammatory response in the lung after inhalation of (1-->3)-beta-D-glucan and bacterial endotoxin.. Guinea pigs were exposed daily to an aerosol of pure (1-->3)-beta-D-glucan and pure endotoxin for five weeks. Lung lavage and lung interstitial cell preparations were done and the inflammatory cells counted. Histological sections were prepared from the trachea.. There was an increase in eosinophil numbers in lung lavage, lung interstitium, and the airway epithelium of animals exposed to (1-->3)-beta-D-glucan. In animals simultaneously exposed to endotoxin, there was no increase in eosinophils. In the lung interstitium, (1-->3)-beta-D-glucan exposure caused an increase in lymphocytes, which was not found after endotoxin exposure. Endotoxin exposure caused an increase in neutrophils and macrophages in lung lavage, which was not found after (1-->3)-beta-D-glucan exposure.. The results support previous findings that (1-->3)-beta-D-glucan causes a different response in the airways as compared to endotoxin. Endotoxin modulated the increase in eosinophils caused by (1-->3)-beta-D-glucan exposure, suggesting a complex interaction between the microbial cell wall components.

Topics: Administration, Inhalation; Air Pollutants; Animals; beta-Glucans; Bronchoalveolar Lavage Fluid; Drug Interactions; Endotoxins; Female; Glucans; Guinea Pigs; Male; Pulmonary Eosinophilia; Tracheal Diseases