What is a result of decreased leukotrienes due to corticosteroids targeting Phospholipase A2?

Corticosteroids are anti-inflammatory agents that target various components of the inflammatory response. One of their mechanisms of action involves inhibiting Phospholipase A2, an enzyme that plays a crucial role in the release of arachidonic acid from cell membrane phospholipids. Arachidonic acid is a precursor for the synthesis of various eicosanoids, including leukotrienes.

Leukotrienes, particularly LTB4, are known to mediate inflammation by promoting leukocyte adhesion, chemotaxis, and activation. When corticosteroids decrease leukotriene production, it leads to reduced recruitment and activation of leukocytes at the site of inflammation. This results in decreased leukocyte adhesion, as fewer inflammatory cells are attracted to the site of injury or infection.

The decrease in leukocyte adhesion is significant because it helps to mitigate the overall inflammatory response, thereby reducing potential tissue damage associated with chronic inflammation. This is especially beneficial in conditions such as asthma, allergic reactions, and autoimmune disorders where excessive inflammation is problematic.

The other choices do not reflect the primary effect of decreased leukotrienes. For instance, decreased leukotrienes would not result in increased eosinophils or lymphocyte counts, as these are more closely related to other