Immunity and Inflammation

Introduction & pharmacological rationale

• Inflammation defined — a physiological, protective response to tissue injury and infection — not a synonym for infection (infection is only one trigger); its purpose is threefold — restrict damage to the localised site, recruit immune cells to eliminate the pathogen, and initiate wound repair.
• The cardinal signs — the four Roman signs — rubor (redness) & calor (heat) from vasodilation; tumor (swelling/oedema) from increased vascular permeability; dolor (pain) from mediators (prostaglandins, bradykinin) sensitising nociceptors — plus a fifth added later, functio laesa (loss of function).
• Central pharmacological principle — almost every soluble mediator or cellular step in the cascade is a druggable target — histamine → antihistamines, eicosanoids → NSAIDs/coxibs/leukotriene modifiers, the arachidonic-acid cascade upstream → glucocorticoids, cytokines → biologicals, leukocyte trafficking → anti-integrins, immune checkpoints → checkpoint inhibitors. This mediator→drug-target map is the exam spine of the topic.
• Scope — this is the mechanistic overview; the detailed pharmacology of the individual anti-inflammatory drug classes (NSAIDs, corticosteroids, antihistamines, immunosuppressants, biologicals) lives in their own topics.