Background: Epidemiologic and experimental studies suggest that air pollution such as diesel exhaust particles (DEPs), one of the important air pollutants, may play a role in the increasing ...prevalence of allergic airway diseases.
Objective: We studied the effect of suspended particulate matter (SPM) and its main component, DEPs, on the production of IL-8 and granulocyte-macrophage colony-stimulating factor (GM-CSF) by human airway epithelial cells in vitro.
Methods: SPM obtained from high-volume air samplers and DEPs were added to cultured human nasal polyp–derived upper airway, normal bronchial, and transformed bronchial epithelial cells. Production of GM-CSF and IL-8 by airway epithelial cells was evaluated.
Results: Nontoxic doses of DEPs showed a significant stimulatory effect on IL-8 and GM-CSF production by these three kinds of epithelial cells in a dose- and time-dependent fashion. SPM had a stimulatory effect on GM-CSF, but not IL-8, production. These effects were abrogated by treatment with a protein synthesis inhibitor, cycloheximide, suggesting that the process required a de novo protein synthesis. On the double-chamber plates, airway epithelial cells responded to DEPs only when they were stimulated from the apical sides, which can be a model for in vivo environments. Neither charcoal nor graphite showed such stimulatory effects, indicating that the activity of DEPs did not derive from their particulate nature. Benzo(a)pyrene, one of the main aromatic hydrocarbons contained in DEPs, showed a stimulatory effect on the release of the cytokines, and this organic substance might have a causative effect on of the potency of DEPs.
Conclusion: We conclude that SPM and DEPs, its main component, might be important air pollutants in the activation of airway epithelial cells for the release of cytokines relevant to allergic airway inflammation. (J Allergy Clin Immunol 1998;101:778-785.)
The /alpha/ parameters and extinction ratios of InGaAsP-InP electroabsorption (EA) modulators and Mach-Zehnder (MZ) modulators are theoretically investigated. The bound states of excitons in quantum ...wells (QWs) under electric field are calculated through the finite-difference method, and quasi-bound states are obtained by the transfer-matrix method. Reducing the heights of the potential barriers of the QWs is prerequisite to achieving small values of the /alpha/ parameter for EA modulators and low driving voltages for MZ modulators. Bulk EA modulators are shown to inherently have relatively small /alpha/ parameters; however, they also require a tradeoff between the extinction ratio and the insertion loss. The /alpha/ parameters of symmetrical and /pi/-phase-shifted MZ modulators in the single- and dual-drive cases are also discussed.
We evaluated the effects of several antibiotics on IL-6 expression by human bronchial epithelial cells, potent sources of this proinflammatory tory cytokine important in airway inflammation. Among ...those tested, erythromycin (EM) and clarithromycin (CAM) uniquely suppressed mRNA levels as well as the release of IL-6 at the therapeutic and non-cytotoxic concentration (10−6M). Our findings suggested that these macrolide antibiotics had suppressive effect on cytokine expression in human cells, and this new mode of action may have relevance to their clinical effectiveness in airway inflammatory diseases.
Epidemiologic and experimental studies suggest that diesel exhaust particles (DEPs) may be related to increasing respiratory mortality and morbidity. We have shown that DEPs augmented the production ...of inflammatory cytokines by human airway epithelial cells in vitro. To better understand the mechanisms of their proinflammatory activities, we studied the effects of several components extracted from DEPs on interleukin (IL)-8 expression in human bronchial epithelial cell line BEAS-2B and normal human airway epithelial cells obtained from very peripheral airways by an ultrathin bronchoscope. We used several agents active on signal transduction pathways in cytokine expression, such as the protein kinase C inhibitor staurosporin, antioxidant agents including N-acetyl cysteine (NAC) and pyrrolidine dithiocarbamate (PDTC), and p38 mitogen-activated protein kinase (MAPK) inhibitor SB203580. Benzene-extracted components showed effects mimicking DEPs on IL-8 gene expression, release of several cytokines (IL-8; granulocyte macrophage colony-stimulating factor; and regulated on activation, normal T cells expressed and secreted) and nuclear factor (NF)-kappa B activation. We also found that NAC, PDTC, and SB203580 suppressed the activities of DEPs and their benzene extracts, suggesting the roles of oxidants-mediated NF-kappa B activation and p38MAPK pathways. Finally, benzoapyrene, one of the important compounds included in the benzene component, replicated the activities shown by DEPs.
An optical modulator based on an InGaAlAs/InGaAlAs multiple quantum well (MQW) structure is demonstrated. The fabricated device had an extinction ratio 6 dB higher than that of a conventional ...InGaAsP-based device with similar chirp behaviour. The InGaAlAs MQW effectively improved the performance trade-off between the extinction ratio and chirping parameter.
Epidemiological and experimental studies suggest that diesel exhaust particles (DEP) may play an active role in the increased respiratory mortality and morbidity. We have shown that DEP augmented the ...production of inflammatory cytokines by human airway epithelial cells in vitro. ICAM‐1 has been shown to play an important role in the local accumulation of inflammatory cells. We studied the effect of DEP on ICAM‐1 gene expression and surface expression in human bronchial epithelial cell line BEAS‐2B. DEP (5–50 μg/ml) showed a stimulatory effect on ICAM‐1 mRNA levels as evaluated by reverse transcription‐polymerase chain reaction (RT‐PCR). Flow cytometric analysis demonstrated an increased ICAM‐1 expression on the epithelial cell surfaces. The soluble form of ICAM‐1 molecules was also increased by the stimulation of DEP. In vitro neutrophil attachment onto DEP‐stimulated epithelial cells was augmented, which was partially blocked by anti‐ICAM‐1 neutralizing antibody. Finally, these events were significantly inhibited by pretreatment with anti‐oxidants pyrrolidine dithiocarbamate and N‐acetyl cysteine, and p38 mitogen activated protein kinase (MAPK) inhibitor SB203580. These findings suggested that DEP induced up‐regulation of ICAM‐1 gene, and this process might be largely dependent on oxidant‐mediated NF‐κB activation and p38‐MAPK pathways.
Erythromycin and its fourteen-member macrolide analogues have attracted attention for their efficacy in bronchial asthma. However, their mechanisms of action remain unclear. We evaluated the effects ...of the macrolide antibiotics on endothelin-1 (ET-1) expression in normal and transformed human bronchial epithelial cells, one of the sources of this potent bronchoconstrictor important in the pathogenesis of asthma. Human bronchial epithelial cells were obtained from the resected bronchi, and the effect of several antimicrobial and antiasthmatic drugs on the production and messenger ribonucleic acid (mRNA) levels of ET-1 was evaluated. Bronchoepithelial cells were also isolated from the mucosa of asthmatic patients under fibreoptic bronchoscopy, and the modulating effects of the drugs were studied. Erythromycin and clarithromycin uniquely suppressed mRNA levels as well as the release of ET- at therapeutic and non-cytotoxic concentrations (percentage inhibition of ET-1 protein release: 26.4+/-5.22% and 31.2+/-7.45%, respectively, at 10(-6) M). Furthermore, erythromycin and clarithromycin inhibited ET-1 expression in bronchoepithelial cells from patients with chronic, stable asthma. A glucocorticosteroid, dexamethasone, also inhibited ET-1 expression. In contrast, theophylline, salbutamol and FK506 had no effect on ET-1 production. Our findings demonstrated that these fourteen-member macrolide antibiotics had an inhibitory effect on endothelin-1 expression in human bronchial epithelial cells. Moreover, this new mode of action may have some relevance to their clinical efficacy in bronchial asthma.
The linewidth enhancement factor alpha of strained quantum-well lasers is analyzed by the k-p perturbation method using the effective-mass approximation. It is found that the alpha factor in a ...strained In/sub 0.80/Ga/sub 0.20/As/InP quantum-well (QW) laser with 1.9% biaxial compression is less than 1.5. For a strained QW laser with p-type modulation doping (MD) of 5*10/sup 18/ cm/sup -3/, the alpha factor is as small as 0.8. It is also demonstrated that the spectral linewidth and wavelength chirping in the strained MD QW laser are significantly less than those in conventional bulk and QW lasers.< >
It has been suggested that eosinophils (Eos) are responsible for damage to bronchial epithelial cells by releasing toxic eosinophil granule proteins in bronchial asthma. We examined eosinophil ...cationic protein (ECP) release from human Eos cultured in the presence of human bronchial epithelial cell line BEAS-2B (Ep). ECP release was potentiated only when both Eos and Ep were activated by IL-5 and TNF, respectively, while it was not potentiated when either Eos or Ep were activated. ECP release from Eos activated by IL-5 was also enhanced when Ep was stimulated by IFN-gamma. Paraformaldehyde fixation of Ep had no effect on ECP enhancement, excluding the possibility that soluble factors from Ep contribute to ECP potentiation. Coculture of Eos and Ep with cytokine treatment resulted in the enhancement of eosinophil adhesion and ECP release, and eosinophil adhesion preceded ECP release in the kinetic study. The enhancement of ECP release was partially inhibited by anti-CD18 mAb, which caused partial and comparable inhibition on the potentiation of eosinophil adhesion. These results suggest that the activation of Ep may profoundly affect the ability of cocultured Eos to release ECP and that CD18-dependent adhesion of Eos to Ep may be considered as one of the mechanisms of ECP enhancement.
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