Table 1.
Changing conceptions of inflammation over the past two decades
| Conception | Detection | Stimuli | Causes of non-resolution or recurrence | Participating cells | Overall function | Therapeutic concerns |
|---|---|---|---|---|---|---|
| 20th centurya,b | macroscopically or microscopically | emergent; usually evident; may be single | persistent stimulus | cells of the immune system | resolve problem or initiate an immune response | infection, trauma, cancer, asthma, atherosclerosis, diabetes, autoimmune disorders, etc. |
| 21st century V.0c,d | macroscopically, microscopically, or inferred from increased production of cytokines, chemokines, non-protein mediators and products they induce | dual stimuli, signaling infection plus injury; or inapparent but seemingly continual stimuli, implied by spontaneous inflammation being a phenotype of numerous gene deficiencies | persistent stimulus; emergent secondary stimulus, such as autoimmune response; excessive or prolonged initial response; subnormal initial response; defective switch of cells and mediators from pro- to anti-inflammatory, depending on context; loss of a constitutively operating anti-inflammatory mechanism | cells of the immune system | resolve problem or initiate an immune response | as for 20th century, with additional focus on metabolic and neurodegenerative diseases |
| 21st century V.1e | “any process involving signals and cells known to orchestrate the more familiar acute inflammatory response” | reaction to a perturbation, or participation “in normal homeostatic processes in the absence of any perturbations” | ||||
| 21st century V.2f | as for V.0 | as for V.0 plus air pollution, temperature extremes, dietary deficiencies, and stresses of poverty and discrimination | as for V.0, with additional recognition of inflammatory memory and inflammaging | any cells, including microbiota | as for V.1, with emphasis on joint participation with the endocrine and nervous systems in providing homeostatic control and restoration | as for V.0, with additional emphasis on inflammatory modulation in immuno-oncology and societal actions to reduce inflammatory inequity |
Cells in the table are unfilled when the topic was not a focus of the article cited.
f
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