Inflammation is a coordinated biological response to infection, tissue injury, or other harmful stimuli. It involves the immune system, blood vessels, and affected tissues, helping remove threats and initiate repair. Although inflammation is normally protective, an excessive, misdirected, or persistent response can damage healthy tissue and contribute to disease. It is a process rather than a single diagnosis, and it may occur locally or involve responses throughout the body. (niehs.nih.gov)
Triggers and recognition
Inflammatory triggers include bacteria, viruses, other infectious organisms, physical injuries, foreign material, chemicals, and radiation. Infection and inflammation are not synonymous: infection involves an infectious organism, whereas inflammation can occur without one, as after a burn or mechanical injury. Such noninfectious responses are often described as sterile inflammation. (ncbi.nlm.nih.gov)
Inflammation begins when biological sensors recognize a harmful stimulus or signals released by damaged cells. These sensors activate pathways that produce inflammatory mediators and recruit cells capable of responding to the threat. This rapid recognition belongs principally to innate immunity, although other immune mechanisms can participate as the response develops. The nature and intensity of inflammation depend on the stimulus, the affected tissue, and the regulation of these pathways. (ncbi.nlm.nih.gov)
Inflammatory responses also occur in autoimmune diseases, in which immune reactions target the body's own components. Rheumatoid arthritis, for example, involves inflammation of joints and surrounding tissues. Persistent inflammation therefore does not necessarily indicate a persistent infection. (ncbi.nlm.nih.gov)
Vascular and cellular mechanisms
During acute inflammation, small blood vessels dilate, increasing blood flow to the affected area. Their permeability also increases, allowing fluid and circulating proteins to enter the tissues. These changes help deliver defensive components but also produce swelling. The local circulation is not merely a transport route: changes in vessel function are integral to initiating and sustaining inflammation. (ncbi.nlm.nih.gov)
Leukocytes, or white blood cells, are recruited from the circulation into affected tissues. Neutrophils commonly predominate early in acute inflammation. Macrophages participate in recognition, inflammatory signaling, and the removal of microbes and cellular debris through phagocytosis. Their activities can both support defense and contribute to tissue damage. (ncbi.nlm.nih.gov)
Inflammatory mediators include cytokines, histamine, and other signaling substances. They influence vascular behavior, immune-cell recruitment, pain, and repair. Cytokines released by activated cells can amplify the response by activating additional cells. In longer-lasting inflammation, adaptive immunity may also contribute through T cells, B cells, and antibodies. These interacting mechanisms explain why different inflammatory conditions have different cellular patterns rather than one uniform response. (ncbi.nlm.nih.gov)
Signs and systemic effects
The five classical signs of acute inflammation are redness, heat, swelling, pain, and loss of function. Increased blood flow accounts for redness and warmth; fluid accumulation contributes to swelling; inflammatory mediators stimulate pain-sensitive nerves. Loss of function can reflect pain, swelling, or disruption of the affected tissue. Not every inflammatory response produces all five signs, and some internal or chronic inflammation has no obvious outward manifestations. (ncbi.nlm.nih.gov)
Severe inflammation can produce systemic effects, including fever, exhaustion, and changes in blood measurements. These may include increased white blood cell counts and increased concentrations of acute-phase proteins. C-reactive protein (CRP), made by the liver, is one such protein; its concentration often rises in response to inflammatory cytokines. Systemic manifestations indicate that the response extends beyond a visibly affected local site. (ncbi.nlm.nih.gov)
Acute and chronic inflammation
Acute inflammation develops rapidly and typically lasts a relatively short time. Its characteristic features include vascular changes and the recruitment of neutrophils. Chronic inflammation persists for months or years and may follow an unresolved acute response or develop through sustained immune activation. Duration alone does not describe its full character: the cellular composition and accompanying tissue changes also differ. (ncbi.nlm.nih.gov)
Chronic inflammation commonly involves macrophages, lymphocytes, and plasma cells, with tissue injury and repair occurring together. Prolonged repair responses can produce fibrosis, the accumulation of scar-like connective tissue. Persistent inflammation is associated with numerous disorders, including inflammatory bowel diseases and some forms of cancer. These relationships differ between diseases; inflammation is not a single explanation for all chronic illness. (ncbi.nlm.nih.gov)
Resolution and tissue repair
Resolution is an active, regulated process rather than simply the exhaustion of an inflammatory response. Signals limit further leukocyte recruitment, while macrophages remove dead cells and debris. Some recruited cells undergo apoptosis, or programmed cell death; others leave through the lymphatic system. These coordinated events support restoration of tissue homeostasis and physiological function. Failure of resolution can allow inflammation to persist. (pubmed.ncbi.nlm.nih.gov)
Clinical assessment
Inflammation is assessed using symptoms, medical history, examination, and laboratory findings. CRP and the erythrocyte sedimentation rate are commonly used inflammatory biomarkers, but neither establishes a specific diagnosis by itself. An elevated CRP concentration does not identify the cause or location of inflammation, and a low concentration does not always exclude it. Interpretation therefore depends on the underlying clinical condition and other evidence, rather than on a single universal “inflammation level.” (medlineplus.gov)