Learning Objective
Describe the defining features, causes, mediators, and outcomes of chronic inflammation.
Chronic inflammation is a prolonged inflammatory response characterized by mononuclear cell infiltration—primarily macrophages, lymphocytes, and plasma cells—with simultaneous tissue destruction and repair, including angiogenesis and fibrosis. It may follow acute inflammation or arise insidiously.
Stimuli (Causes)
- Persistent infections
- Examples: Mycobacterium tuberculosis, Treponema pallidum, certain fungi and viruses
- Type IV (delayed-type) hypersensitivity
- Autoimmune diseases
- Prolonged exposure to toxic agents (eg, silica)
- Foreign materials
Activity
Key Mediators
- Macrophages are the dominant effector cells in chronic inflammation.
- Sustained inflammation is driven by reciprocal activation of macrophages and T lymphocytes:
- Th1 cells → secrete IFN-γ → classical macrophage activation (proinflammatory, microbicidal)
- Th2 cells → secrete IL-4 and IL-13 → alternative macrophage activation (tissue repair, fibrosis, anti-inflammatory effects)
Outcomes
- Fibrosis and scarring
- Amyloidosis
- Neoplastic transformation due to persistent inflammation:
- Chronic HCV infection → chronic hepatitis → hepatocellular carcinoma
- Helicobacter pylori infection → chronic gastritis → gastric adenocarcinoma
