TY - JOUR
T1 - Antiinflammatory therapies other than corticosteroids.
AU - Rennard, Stephen I.
PY - 2004
Y1 - 2004
N2 - Antiinflammatory therapy for chronic obstructive pulmonary disease (COPD) can be directed at several stages of the inflammatory process. Much attention has been focused on blocking the damaging effects of toxic mediators released by inflammatory cells, including antioxidants and antiproteases. An alternate strategy is to block the recruitment of inflammatory cells into the lung, such as by inhibiting the production of chemotactic factors driving inflammatory cell recruitment, the ability of inflammatory cells to respond to chemotactic factors, and the ability of inflammatory cells to migrate. Moreover, mediators released by inflammatory cells, particularly tumor necrosis factor-alpha, probably have systemic effects in COPD. Blocking the release of these cytokines or blocking their ability to act on distal tissues represents another potential therapeutic option. It is also important to recognize that the various components of the inflammatory response are not independent. The action of proteases released by inflammatory cells, for example, can generate chemotactic factors, lead to activation of inflammatory cells, and modulate repair responses. The complex network of regulatory molecules that controls the inflammatory response, therefore, presents a number of potential therapeutic targets with the promise of altering the disease process in COPD.
AB - Antiinflammatory therapy for chronic obstructive pulmonary disease (COPD) can be directed at several stages of the inflammatory process. Much attention has been focused on blocking the damaging effects of toxic mediators released by inflammatory cells, including antioxidants and antiproteases. An alternate strategy is to block the recruitment of inflammatory cells into the lung, such as by inhibiting the production of chemotactic factors driving inflammatory cell recruitment, the ability of inflammatory cells to respond to chemotactic factors, and the ability of inflammatory cells to migrate. Moreover, mediators released by inflammatory cells, particularly tumor necrosis factor-alpha, probably have systemic effects in COPD. Blocking the release of these cytokines or blocking their ability to act on distal tissues represents another potential therapeutic option. It is also important to recognize that the various components of the inflammatory response are not independent. The action of proteases released by inflammatory cells, for example, can generate chemotactic factors, lead to activation of inflammatory cells, and modulate repair responses. The complex network of regulatory molecules that controls the inflammatory response, therefore, presents a number of potential therapeutic targets with the promise of altering the disease process in COPD.
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U2 - 10.1513/pats.200402-020MS
DO - 10.1513/pats.200402-020MS
M3 - Review article
C2 - 16113447
AN - SCOPUS:26944469101
SN - 1546-3222
VL - 1
SP - 282
EP - 287
JO - Proceedings of the American Thoracic Society
JF - Proceedings of the American Thoracic Society
IS - 3
ER -