Inflammatory cytokines, prostaglandins, and leukotrienes

Inflammatory cytokines, prostaglandins, and leukotrienes is a collective term for several distinct classes of endogenous signaling molecules that drive the inflammatory process [1]. Cytokines, including tumor necrosis factor (TNF) and various interleukins (ILs), are proteins that mediate cell-to-cell communication in the immune system [2]. Prostaglandins and leukotrienes are lipid-derived eicosanoids synthesized from arachidonic acid via the cyclooxygenase (COX) and lipoxygenase (LOX) pathways, respectively [3]. These mediators are involved in a wide range of physiological and pathological processes, such as vasodilation, pain sensitization, and the recruitment of leukocytes to sites of injury [4]. Because this grouping encompasses multiple unrelated molecular families and distinct pharmacological targets, it is considered a broad category of inflammatory mediators rather than a single therapeutic target [5]. Drugs that interact with these pathways include nonsteroidal anti-inflammatory drugs (NSAIDs), leukotriene modifiers, and biologic agents like TNF inhibitors [6].

Other names

Inflammatory mediatorsPro-inflammatory signaling moleculesEicosanoids and cytokines

Therapeutic agents modulate these pathways through several distinct mechanisms: NSAIDs inhibit cyclooxygenase (COX) enzymes to reduce prostaglandin synthesis; leukotriene receptor antagonists (LTRAs) block the CysLT1 receptor; 5-LOX inhibitors prevent leukotriene production; and biologic therapies (e.g., monoclonal antibodies) neutralize specific pro-inflammatory cytokines such as TNF-alpha, IL-1, or IL-6 [3, 5, 6].