Grain dust induces IL-8 production from bronchial epithelial cells: the effect of dexamethasone on IL-8 production

Park, Hae‐Sim; Suh, Jung-Hee; Kwon, O Jung; Choi, Dong-Chull

doi:10.1016/s1081-1206(10)63286-3

Cited by 4 publications

(3 citation statements)

References 15 publications

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“…The effects of IL-18 on immune function are essentially opposite to that of GCs. IL-18 is a proinflammatory cytokine which stimulates the production of TNF-· and subsequently that of IL-1ß and IL-8 [16,17], whereas GCs inhibit the synthesis of these cytokines [18][19][20]. IL-18 is also a modulator of the Th1/Th2 balance.…”

Section: Introductionmentioning

confidence: 99%

Modulation of IL-18 Production in the Adrenal Cortex following Acute ACTH or Chronic Corticosterone Treatment

Conti

Sugama

Kim

et al. 2000

Neuroimmunomodulation

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Interleukin (IL)-18 is a proinflammatory cytokine and a stimulator of cell-mediated immune responses. We have previously reported that acute stress stimulates the production of IL-18 mRNA in the glucocorticoid (GC)-producing cells of the adrenal cortex. In order to investigate the mechanisms governing the expression of IL-18 in the adrenal cortex, the effects of acute ACTH or chronic corticosterone treatment on the levels of IL-18 mRNA and protein were examined by in situ hybridization and Northern and Western blot assays. Adult male Sprague-Dawley rats received a subcutaneous injection of ACTH or subcutaneous implantation of slow-release corticosterone pellets followed by an injection of saline or ACTH. After 4 h, ACTH induced a 4-fold increase in IL-18 mRNA levels and elevated the content of pro-IL-18 peptide. Six days of chronic corticosterone treatment did not alter the basal levels of IL-18 mRNA and reduced those of pro-IL-18. Finally, ACTH treatment of animals under the corticosterone regimen induced a 2-fold increase in IL-18 mRNA and elevated the levels of the pro-IL-18 protein. The levels of the precursor, p45, and the active subunit p10 peptides of the IL-18-processing enzyme, IL-1β-converting enzyme (ICE), showed no substantial differences in all the conditions tested. IL-1β was not detected under these experimental conditions. These data demonstrate that the production of IL-18 in the adrenal cortex is stimulated by ACTH treatment and is not inhibited by the direct action of corticosterone. In contrast to the anti-inflammatory action of GCs, IL-18 may have an immunostimulatory role during acute stress.

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Section: Introductionmentioning

confidence: 99%

Modulation of IL-18 Production in the Adrenal Cortex following Acute ACTH or Chronic Corticosterone Treatment

Conti

Sugama

Kim

et al. 2000

Neuroimmunomodulation

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“…Specifically, glucocorticoids with anti-inflammatory potential, such as dexamethasone, have been shown to repress interleukin-6 gene expression in a NF-B-dependent mechanism (53). Other research has established similar results with regard to TNF-␣, IL-1␤, IL-8, and IL-16 (54)(55)(56)(57)(58)(59)(60)(61). These same cytokines have been indicated in the depression of cardiac efficiency via an NO-dependent pathway (62).…”

Section: Discussionmentioning

confidence: 80%

Modulation of the Inflammatory Response in the Cardiomyocyte and Macrophage

Sanders

Hunter

et al. 2001

J Extra Corpor Technol

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Numerous cardiac disease processes have been linked to the overproduction of nitric oxide (NO) via inducible nitric oxide synthase (iNOS) in the cardiovascular system. Chronic and acute exposure to hyperphysiologic levels of NO has been suggested as an agent in chronic transplant rejection, various cardiomyopathies, reperfusion injury, and the inflammatory state following cardiopulmonary bypass. Proinflammatory cytokines and inflammatory cell types, such as macrophage and neutrophils, have also been implicated in the pathophysiology associated with the previously mentioned syndromes. Previous work by this group has shown that lipopolysaccharide (LPS) in combination with tumor necrosis factor-α (TNF-α) can increase iNOS expression and the production of NO in macrophage. With this in mind, we hypothesized that increased iNOS expression and NO production generated by LPS and TNF-α in the macrophage could be mimicked in the cardiomyocyte and potentially account for some aspect of the cardiac dysfunction attributed to NO. Furthermore, this increased expression of iNOS and NO production could be returned to control using the glucocorticoid, dexamethasone, a known iNOS transcription blocker. Using fetal rat cardiomyocytes in primary culture cell line and a murine macrophage cell line, RAW 264.7, the expression of iNOS was quantified with specific FITC-conjugated antibodies using fluorescence activated cell sorter (FACS) and NO production with a Bioxytech nitric oxide spectrophotometric assay. The myocytes and macrophage were separated into three groups, Control, TNF + LPS, and (+) Dexamethasone. The control groups received no TNF or LPS or dexamethasone, TNF + LPS groups received TNF-α and LPS for 8 hours with no dexamethasone, and the (+) Dexamethasone groups were pretreated with dexamethasone for 8 hours and stimulated with TNF-α and LPS along with a second 8-hour treatment of dexamethasone. The macrophage cell groups treated with TNF-α and LPS showed a 335% increase over control in iNOS expression, and NO production was increased 494% from control. Macrophage treated with dexamethasone experienced an attenuation of iNOS expression of 200% toward control from stimulated levels and 202% decrease in NO production from stimulated levels toward control. Cardiomyocytes exhibited no statistically significant change in the expression of iNOS or NO production with stimulation or dexamethasone treatments. In conclusion, iNOS and NO were elevated in macrophage, which can be blunted in the presence of dexamethasone in the macrophage. Curiously, iNOS could not be stimulated in the cardiomyocyte, suggesting inflammatory cells may be largely responsible for the elevated iNOS and NO experienced in some cardiovascular diseases. The clinical relevance of this study is the introduction of specific iNOS inhibitors into the cardiopulmonary bypass circuit could serve as a potential mechanism for modulating the inflammatory response surrounding cardiopulmonary bypass. Likewise, therapeutic glucocorticoid administration could improve outcomes for patients with inflammatory cardiovascular disease states related to elevated NO production.

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“…LPS is reported to induce eosinophil accumulation (Peden et al 1999, Penido et al 2001) and prolong eosinophil survival (Meerschaert et al 2000). Furthermore, grain dust inhalation induces IL-8 production by bronchial epithelial cells, and increases polymorphonuclear cell accumulation in the airway (Becker et al 1999;Park et al 1999). Thus, LPS contained in rice-husk dust acts on cells orchestrating airway inflammation.…”

Section: Discussionmentioning

confidence: 99%

Activation of Eosinophils by Rice-Husk Dust Exposure: A Possible Mechanism for the Aggravation of Asthma during Rice Harvest

Kayaba

Meguro

Muto

et al. 2004

Tohoku J. Exp. Med.

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Grain dust and other irritants affect the airway of allergic patients in rice-growing area during the harvest. The aim of this study was to elucidate the mechanism of airway hypersensitivity in rice-growing areas during the harvest. Firstly, the effect of rice-husk dust on eosinophil activation was studied. Secondary, the concentration of lipopolysaccharides (LPS), a potent activator of inflammatory cells, in rice-husk dust was measured. Since it is possible for LPS, a component of gram-negative bacterial cell wall, to adhere to the particle of smoke generated from rice-husk dust, LPS contained in the smoke was also measured. Furthermore, chemical irritants contained in the smoke generated from the rice-husk dust were analyzed. Microscopically, the dust contained fine thorns dropped off from the outer sheath of the rice, and irritated the skin, throat and eyes. The grain dust extract increased the expressions of eosinophil activation markers. These up-regulatory effects were largely dependent on LPS. The smoke contained LPS and several chemical irritants such as formaldehyde and acetaldehyde. Rice-husk dust and its smoke, hazardous air pollutants, probably play a major role in the aggravation of airway diseases in agricultural areas.

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Grain dust induces IL-8 production from bronchial epithelial cells: the effect of dexamethasone on IL-8 production

Cited by 4 publications

References 15 publications

Modulation of IL-18 Production in the Adrenal Cortex following Acute ACTH or Chronic Corticosterone Treatment

Modulation of IL-18 Production in the Adrenal Cortex following Acute ACTH or Chronic Corticosterone Treatment

Modulation of the Inflammatory Response in the Cardiomyocyte and Macrophage

Activation of Eosinophils by Rice-Husk Dust Exposure: A Possible Mechanism for the Aggravation of Asthma during Rice Harvest

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