炎症反应双通道幻灯片.pptVIP

SGA 2003-W-6701-SS MS* Slide 5 Corticosteroids can influence the regulation of numerous mediatorsof the inflammatory process, including cytokines (ILs 1–8, 11–13), tumor necrosis factor-alpha, granulocyte macrophage colony-stimulating factor, adhesion molecules (intracellular adhesion molecule-1, vascular-cell adhesion molecule-1), and inducible enzymes (nitrogen oxide synthase and cyclo-oxygenase [COX]-2).7 These drugs, however, may act unpredictably on many inflammatory processes. The effects of corticosteroids on leukotriene synthesis depend on the cell type and whether the drugs are administered in vivo or in vitro. While phospholipase A2 activity may be inhibited, increased expression of 5-lipoxygenase or 5-lipoxygenase–activating protein is also possible and may lead to different effects in different patients, depending on which steps in the pathway are rate-limiting and the extent to which each step can be modulated. Moreover, by inhibiting COX-2 and thereby prostaglandin E2, which inhibits leukotriene synthesis, corticosteroids may indirectly amplify leukotriene synthesis.7 SGA 2003-W-6701-SS MS* Slide 3 A recent study examined the relationship between airway inflammation and disease activity in 74 non-smoking patients with intermittent (n=19), mild to moderate (n=38), or severe persistent (n=17) asthma. Twenty-two nonatopic individuals served as controls. A subanalysis（亚组分析） was performed of patients receiving corticosteroid therapy. Patients with mild to moderate asthma showed significantly higher levels of inflammatory mediators (eosinophils) versus controls, despite treatment with high (p0.01) or low (p0.001) doses of inhaled corticosteroids (ICS). Similarly, patients with severe asthma receiving oral corticosteroids or oral corticosteroids + ICS showed significantly higher eosinophil counts than controls (p0.01).3 Thus, some degree of airway inflammation may persist despite treatment with corticosteroids at any dose. 最近一项在74名不吸烟的患者的研究调查了气道炎症和疾