Effects of Short-Term Nitrogen Monoxide Inhalation on Leukocyte Adhesion Molecules, Generation of Reactive Oxygen Species, and Cytokine Release in Human Blood

Opdahl, Helge; Haugen, Torbjørn; Hagberg, Inger Anne; Aspelin, Trude; Lyberg, Torstein

doi:10.1006/niox.2000.0275

Cited by 4 publications

(1 citation statement)

References 84 publications

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“…However, leukocyte surface receptor expression was not analyzed in this study (35). Others investigators did not observe any change in CD11a, CD11b, CD11c, and CD62L expression after a 35-min breathing period of 40 ppm inhaled NO in 30% oxygen in a relatively small study population of eight healthy volunteers (36). In contrast, a reduction in both spontaneous H 2 O 2 release and CD11/CD18 expression was observed in PMN from bronchoalveolar lavage during the inhalation of 18 ppm NO and significantly higher oxygen concentrations in patients with ARDS (20).…”

Section: Discussionmentioning

confidence: 63%

Inhaled nitric oxide inhibits platelet-leukocyte interactions in patients with acute respiratory distress syndrome

Gries

Herr

Kirsch

et al. 2003

Critical Care Medicine

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Section: Discussionmentioning

confidence: 63%

Inhaled nitric oxide inhibits platelet-leukocyte interactions in patients with acute respiratory distress syndrome

Gries

Herr

Kirsch

et al. 2003

Critical Care Medicine

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The molecular biology of nasal polyposis

Bernstein

2001

Curr Allergy Asthma Rep

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The molecular biologic events in the development of nasal polyps are now becoming unraveled. It appears that eosinophils are the dominant inflammatory cell present in this tissue. The events leading up to the extravasation of eosinophils into the lamina propria nasal polyps are regulated by the proinflammatory cytokines tumor necrosis factor-alpha and interleukin-1 beta. These cytokines upregulate very late antigen-4 on the surface of eosinophils and vascular cell adhesion molecule-1 on the surface of the endothelial blood vessel. Chemokines such as RANTES (regulated upon activation, normal T-cell expressed and secreted) and eotaxin are responsible for the movement of eosinophils into the lamina propria of the nasal polyp. The release of major basic protein has an effect on alteration of the epithelial architecture and on the sodium and chloride flux into and out of the apical epithelial cell of the tissue. Finally, the alteration of the surface epithelium results in a defect in the migration of the cystic fibrosis transmembrane regulator protein to the apical surface. These two events, the release of major basic protein from the eosinophil and the alteration of the architecture of the surface epithelium, lead to an increase in sodium absorption and resultant edema: the hallmark of the pathology of the nasal polyp.

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Nitric oxide regulates interactions of PMN with human brain microvessel endothelial cells

Wong¹,

Prameya²,

Dorovini-Zis³

et al. 2004

Biochemical and Biophysical Research Communications

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Effects of Short-Term Nitrogen Monoxide Inhalation on Leukocyte Adhesion Molecules, Generation of Reactive Oxygen Species, and Cytokine Release in Human Blood

Cited by 4 publications

References 84 publications

Inhaled nitric oxide inhibits platelet-leukocyte interactions in patients with acute respiratory distress syndrome

Inhaled nitric oxide inhibits platelet-leukocyte interactions in patients with acute respiratory distress syndrome

The molecular biology of nasal polyposis

Nitric oxide regulates interactions of PMN with human brain microvessel endothelial cells

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