Inhibition of cyclooxygenase by NSAIDs shifts eicosanoid production toward which mediators, promoting bronchoconstriction?

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Multiple Choice

Inhibition of cyclooxygenase by NSAIDs shifts eicosanoid production toward which mediators, promoting bronchoconstriction?

Inhibiting cyclooxygenase blocks the pathway that converts arachidonic acid into prostaglandins and thromboxanes. With COX activity reduced, more arachidonic acid is available for the lipoxygenase pathway, increasing the production of leukotrienes. Leukotrienes, especially LTC4, LTD4, and LTE4, are potent bronchoconstrictors that contract airway smooth muscle and promote mucus production, leading to bronchospasm. This shift helps explain why NSAIDs can provoke bronchoconstriction in susceptible individuals (as seen in aspirin-exacerbated respiratory disease). Lipoxins are anti-inflammatory mediators from LOX, and prostaglandins/thromboxanes are COX products, so the key mediators promoted by this shift toward LOX metabolism are leukotrienes.

Inhibiting cyclooxygenase blocks the pathway that converts arachidonic acid into prostaglandins and thromboxanes. With COX activity reduced, more arachidonic acid is available for the lipoxygenase pathway, increasing the production of leukotrienes. Leukotrienes, especially LTC4, LTD4, and LTE4, are potent bronchoconstrictors that contract airway smooth muscle and promote mucus production, leading to bronchospasm. This shift helps explain why NSAIDs can provoke bronchoconstriction in susceptible individuals (as seen in aspirin-exacerbated respiratory disease). Lipoxins are anti-inflammatory mediators from LOX, and prostaglandins/thromboxanes are COX products, so the key mediators promoted by this shift toward LOX metabolism are leukotrienes.

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