Chronic obstructive pulmonary disease with steroid-resistant.docVIP

Chronic obstructive pulmonary disease with steroid-resistant.doc

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 PAGE \* MERGEFORMAT 14 Chronic obstructive pulmonary disease with steroid-resistant Keywords: chronic obstructive pulmonary disease, glucocorticoid Although glucocorticoids are widely used for chronic infection and immune diseases, but not for all patients are valid. Is well known that asthma and chronic obstructive pulmonary disease (COPD) in their airway had occurred in the activation of the inflammatory process, for asthma patients, glucocorticoid is effective for most patients, and for COPD patients, the hormone very limited [1]. A steroid-resistant A variety of clinical treatment methods for the treatment of COPD is very limited, and currently no effective treatment can slow the progress of COPD. The long-term high-dose inhaled steroid can not slow down the accelerated airway obstruction [2]. For most asthma patients, low doses of inhaled corticosteroids can suppress airway inflammation, and for COPD patients, even the high-dose inhaled or oral corticosteroids are difficult to reduce a variety of inflammatory cells, cytokines, or proteases [ 3 ~ 5]. Alveolar macrophages through the release of proteases such as matrix metalloproteinase-9 (MMP-9), inflammatory factors such as TNF-α, and chemokines such as IL-8 in COPD such as chronic inflammation plays an important synergy. Studies have shown that in healthy non-smoking population of alveolar macrophages, glucocorticoids can effectively inhibit the inflammatory mediators which, in normal lung alveolar macrophages of smokers, its role is limited, while in the COPD patients with alveolar macrophages, the basic no such effect [6 ~ 7]. This research suggests that in COPD patients, the alveolar macrophages of the existence of glucocorticoid resistance. Therefore, to further clarify the molecular mechanisms of hormone resistance might lead to new treatments. Two hormones in the role of inflammation In asthma, hormone off the molecular mechanism of inflammatory gene expressi

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