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Review
. 2006 May;290(5):L797-805.
doi: 10.1152/ajplung.00513.2005.

Involvement of cyclooxygenase-2 and prostaglandins in the molecular pathogenesis of inflammatory lung diseases

Gye Young Park  1 , John W Christman
Affiliations
Review

Involvement of cyclooxygenase-2 and prostaglandins in the molecular pathogenesis of inflammatory lung diseases

Gye Young Park et al. Am J Physiol Lung Cell Mol Physiol. 2006 May.

Abstract

Inducible cyclooxygenase (COX-2) and its metabolites have diverse and potent biological actions that are important for both physiological and disease states of lung. The wide variety of prostaglandin (PG) products are influenced by the level of cellular activation, the exact nature of the stimulus, and the specific cell type involved in their production. In turn, the anti- and proinflammatory response of PG is mediated by a blend of specific surface and intracellular receptors that mediate diverse cellular events. The complexity of this system is being at least partially resolved by the generation of specific molecular biological research tools that include cloning and characterization of the enzymes distal to COX-2 and the corresponding receptors to the final cellular products of arachidonic metabolism. The most informative of these approaches have employed genetically modified animals and specific receptor antagonists to determine the exact role of specific COX-2-derived metabolites on specific cell types of the lung in the context of inflammatory models. These data have suggested a number of cell-specific, pathway-specific, and receptor-specific approaches that could lead to effective therapeutic interventions for most inflammatory lung diseases.

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Figures

Fig. 1
Fig. 1
Schematic summary of PGE2 and PGD2 involvement in allergic inflammatory airway diseases. Th2, T helper type 2.
Fig. 2
Fig. 2
The switching of cyclooxygenase-2 metabolite during the lung inflammatory process. Image illustrates the early phases of inflammatory reaction are leads to early production of prostaglandins, which usually increase the inflammatory reaction by recruiting inflammatory cells and vasodilatation. However, in later stages of the inflammatory reaction, more cyclopentenone prostaglandin 15-deoxy-12,14 PGJ2 (15d-PGJ2) and lipoxin A4 (LXA4) are produced and facilitate the resolution. PPARγ, perxoisome proliferator-activated receptor-γ, TXA2, thromboxane A2.
See this image and copyright information in PMC

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