Immunology of acute vs. chronic inflammation

Acute inflammation is induced by tissue damage due to trauma, noxious compounds, or microbial invasion. The process of acute inflammation is mediated by immune cells, important cell-signaling proteins called cytokines, and other small molecules. Anaphylatoxins, small immune-mediating molecules released at the site of inflammation, stimulate mast cells to release histamine, serotonin and prostaglandins, which cause blood vessels to expand (vasodilation) and become more permeable. This response allows immune cells such as neutrophils to migrate into affected tissue through the capillary wall (diapedesis) and respond to the offending agent (Figure 1). Neutrophils are the major component of pus; additional clinical signs of acute inflammation include swelling, redness, pain and heat at the site of the insult.

Chronic inflammation, in contrast, may be the only inflammatory response seen in certain viral infections and hypersensitivity reactions, particularly if the cause of inflammation is persistent (Table 1). In chronic inflammation, the primary immune cells are macrophages and T lymphocytes, which produce cytokines and enzymes that cause more lasting damage to cells. In chronic inflammation, resolution of the acute infection gives way to ongoing tissue damage and destruction, manifesting as tissue fibrosis.

Adapted from Kantari et al. The role of neutrophils and monocytes in innate immunity. Contrib Microbiol. 2008;15:118-46

Molecules involved in both acute and chronic inflammation have been studied as targets for pharmacologic interventions. Rilonacept, a monoclonal antibody against interleukin-1, was studied in a randomized controlled trial as a treatment option for patients with cyclic fever syndromes, which cause acute inflammatory episodes. In 12 patients who completed two 3-month courses of rilonacept versus 10 patients who had two 3-month courses of placebo, the frequency of patients’ fever episodes was 0.77 versus 2 per month, respectively (p=0.027). The duration of attacks was 1.2 versus 2.4 days in rilonacept and placebo patients, respectively (p=0.32).