Currently, most drugs either inhibit the synthesis of prostaglandins/leukotriene

Question

Currently, most drugs either inhibit the synthesis of prostaglandins/leukotrienes (cyclo-oxygenase inhibitors) or they inhibit transcription of genes encoding inflammatory cytokines (such as IL-1, TNF-beta) (glucacorticoids). present some ideas for new targets for anti-inflammatory drugs that will work by inhibiting extravasation of macrophages, neutrophils, or TH1 cells. Explain the reason choosing a particular target. Then, explain what the target does and explain why inhibiting it will have the effect you expect. Also briefly discuss about possible adverse effects-would the drug cause increased susceptibility to new infections, for example.

Explanation / Answer

A particular target would be Integrins present on leukocytes. Integrins are usually present in an inactive state with low affinity for receptors on endothelial cells of the blood vessel. When these integrins are activated by cytokines they switch from low affinity to high affinity. This results in the binding of integrins to the receptors on the endothelial cells.This causes immobilisation of the leukocytes. This immobilisation is a vital step in the inflammatory process. Unless immobilisation occurs, these leukocytes cannot move into the tissues by extravasation. -------------------- Hence if we mutate the integrins such that they have no affinity for endothelial cells at all, extravasation can be prevented. -------------------- The adverse effects would be an absence of an inflammatory response. In the absence of an inflammatory response, wounds and infections would never heal. Inflammation initiates the healing process.

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