Inflammation is a coordinated biological response to infection, tissue injury, cellular stress, or other forms of harmful stimulation. Its primary purpose is to detect and contain a threat, remove damaged material, initiate repair, and restore tissue function. Inflammation can be acute, developing over minutes to hours, or chronic, persisting for weeks, months, or years. Acute inflammation commonly involves increased blood flow, increased vascular permeability, recruitment of neutrophils, and release of mediators such as histamine, prostaglandins, leukotrienes, cytokines, and complement fragments. Chronic inflammation involves persistent immune activation and can feature macrophages, lymphocytes, tissue remodelling, angiogenesis, and fibrosis. Inflammation is therefore a physiological defence process that becomes harmful when it is excessive, prolonged, misdirected, or unable to resolve appropriately.
The initial inflammatory response involves recognition of danger-associated molecular patterns released by damaged cells and pathogen-associated molecular patterns associated with microorganisms. Pattern-recognition receptors on immune and tissue cells detect these signals and initiate intracellular pathways that alter gene expression and mediator release. Histamine can increase vascular permeability and contribute to vasodilation, while cytokines such as tumour necrosis factor, interleukin-1, and interleukin-6 coordinate local and systemic responses. Chemokines guide leukocytes towards affected tissues. Eicosanoids, including prostaglandins and leukotrienes, influence pain, fever, vascular responses, bronchoconstriction, and leukocyte activity. The inflammatory response is therefore generated by a network of interacting mediators rather than by one single chemical or cell type.
Acute inflammation has recognisable vascular and cellular stages. Arteriolar vasodilation increases local blood flow, contributing to redness and warmth, while increased vascular permeability permits plasma proteins and fluid to move into tissues, producing swelling. Leukocytes initially undergo margination and rolling along activated endothelium, followed by firm adhesion and migration through the vascular wall. Neutrophils are commonly among the earliest recruited leukocytes in acute bacterial inflammation, although the precise cellular pattern varies with the stimulus. Phagocytes then ingest microorganisms, dead cells, and debris and use antimicrobial mechanisms to destroy them. The classic clinical features of inflammation are redness, heat, swelling, pain, and loss of function, although not every inflammatory process produces all five features visibly.
Chronic inflammation differs from acute inflammation in duration, cellular composition, and tissue consequences. Macrophages, lymphocytes, plasma cells, and other immune cells can accumulate in chronically inflamed tissue. Persistent inflammatory signalling can stimulate fibroblasts, extracellular-matrix deposition, angiogenesis, and tissue remodelling. Chronic inflammation contributes to many diseases, including inflammatory bowel diseases, rheumatoid arthritis, atherosclerosis, chronic lung disorders, and some cancers. It can result from persistent infection, autoimmune reactions, prolonged exposure to irritants, metabolic disturbances, or failure to resolve an initial inflammatory response. Chronic inflammation is not simply "acute inflammation lasting longer"; its cellular and molecular environment can become substantially different as the tissue adapts to prolonged immune stimulation.
Resolution is an active biological process rather than merely the passive disappearance of inflammation. Once the original threat is controlled, inflammatory signalling can shift towards termination and tissue repair. Neutrophil recruitment declines, existing neutrophils undergo apoptosis, macrophages clear dead cells, and specialised pro-resolving mediators help coordinate restoration of tissue homeostasis. Fibroblasts and other structural cells participate in repair, while excessive repair can produce fibrosis and permanent architectural changes. Failure of resolution can contribute to chronic inflammatory disease. This distinction is important because suppressing inflammation indiscriminately is not always equivalent to restoring healthy tissue function; some inflammatory activity is necessary for effective host defence and repair.
Inflammation can affect the entire body as well as individual tissues. Systemic release of inflammatory mediators can produce fever, fatigue, changes in appetite, altered metabolism, and increased production of acute-phase proteins by the liver. Severe systemic inflammation can progress to widespread vascular and organ dysfunction, particularly when triggered by serious infection or major tissue injury. Laboratory markers such as C-reactive protein and erythrocyte sedimentation rate can provide indirect evidence of inflammation, but they do not identify its cause by themselves. Elevated inflammatory markers can occur in infection, autoimmune disease, injury, cancer, and many other conditions. Consequently, inflammation should be interpreted as a biological process rather than a diagnosis.
Treatment depends on the cause, location, severity, and consequences of inflammation. Anti-inflammatory medicines include non-steroidal anti-inflammatory drugs, corticosteroids, and numerous targeted biological or small-molecule therapies. NSAIDs reduce production of certain prostaglandins through cyclo-oxygenase inhibition, while corticosteroids broadly alter transcription of inflammatory genes. Targeted therapies can inhibit specific cytokines, immune-cell pathways, or intracellular signalling mechanisms. However, reducing inflammation can also reduce protective immune functions and increase susceptibility to infection or impair tissue repair. Effective management therefore requires addressing the underlying cause whenever possible rather than simply suppressing inflammatory symptoms indefinitely.
Inflammation is closely related to, but distinct from, infection. Infection is caused by an infectious organism, whereas inflammation is a host response that can occur with or without infection. Inflammation can also be protective or pathological depending on context. A common misconception is that inflammation is always harmful and should always be eliminated; acute inflammation is essential for controlling many infections and initiating repair.
Another misconception is that visible swelling is required for inflammation, whereas substantial inflammatory processes can occur internally or at microscopic levels. The modern concept of inflammation developed from anatomical and pathological observations into a molecular discipline involving innate immunity, adaptive immunity, vascular biology, metabolism, tissue repair, and cell signalling.
