Inflammation

Disease / Phenomenon

Inflammation is the body's coordinated response to injury, infection, or irritation, and in its acute form it is protective and self-limiting: blood flow increases, immune cells are recruited, pathogens and damaged tissue are cleared, and repair begins. The classical signs — redness, heat, swelling, pain, and loss of function — reflect this deliberate mobilization. Problems arise when the response fails to resolve. Chronic low-grade inflammation persists quietly for years without obvious symptoms and is now recognized as a common thread running through cardiovascular disease, type 2 diabetes, obesity, arthritis, neurodegeneration, autoimmune conditions, and many cancers, which is why it is often treated as a phenomenon in its own right rather than merely a symptom.

The molecular machinery is well characterized. Pattern recognition receptors, including the Toll-like receptors, detect microbial and damage-associated signals and activate NF-kB and MAPK cascades, driving transcription of TNF-alpha, IL-1beta, IL-6, and chemokines. The NLRP3 inflammasome processes IL-1beta and IL-18. Arachidonic acid is converted by COX-1, COX-2, and lipoxygenase enzymes into prostaglandins and leukotrienes. Resolution is active, mediated by lipoxins, resolvins, protectins, and IL-10. Oxidative stress and NRF2 signaling modulate the balance. This page decomposes inflammation into these processes, pathways, and biomarkers.