Inflammation is the body’s coordinated response to harmful stimuli such as pathogens, toxins or tissue injury. It is essential for survival but can become damaging when persistent or uncontrolled. Research distinguishes two broad types: acute and chronic inflammation.

Acute inflammation begins within minutes or hours after injury. Damaged cells and immune sentinels detect danger signals and release mediators such as histamine, prostaglandins and cytokines. These substances dilate blood vessels, increase vascular permeability and attract immune cells, especially neutrophils and monocytes. The classic signs are redness, heat, swelling, pain and loss of function. Normally, specialized pro resolving mediators then drive the resolution phase, clearing debris and promoting tissue repair, which prevents ongoing damage.

Chronic inflammation arises when the initial trigger persists or when resolution fails. It is characterized by long term recruitment of macrophages and lymphocytes, ongoing production of inflammatory cytokines and progressive tissue remodeling or destruction. This state is closely linked to many major diseases, including atherosclerosis, type 2 diabetes, neurodegenerative disorders, inflammatory bowel disease and certain cancers. Low grade systemic inflammation in particular correlates with metabolic and cardiovascular risk.

Molecular studies emphasize tightly regulated signaling pathways such as NF kappa B, inflammasomes and pattern recognition receptors. Genetic factors, diet, microbiome composition, environmental exposures and stress can modulate these pathways. Current research explores targeted therapies that dampen harmful inflammatory signaling or enhance resolution without broadly suppressing immunity. Lifestyle interventions, including dietary patterns that reduce inflammatory mediators and support a healthy microbiome, are also active areas of investigation.