Acute vs Chronic Inflammation

Acute inflammation is the stereotyped local response to injury or infection: vasodilation, increased permeability and neutrophil influx within hours. Its defining feature is that it is programmed to stop, and resolution is active rather than passive, driven by pro-resolving mediators such as lipoxins and resolvins and by macrophages switching from killing microbes to clearing apoptotic neutrophils. Chronic inflammation is what remains when that switch fails: a mononuclear infiltrate persisting for months or years, with tissue destruction and repair running at once.

An acute bacterial infection can drive C-reactive protein from under 1 mg/L to over 300 mg/L, peaking around 48 hours, while chronic low-grade inflammation sits in the hs-CRP range of 1 to 3 mg/L and barely moves. That low-grade state is not merely a marker: in CANTOS, canakinumab, an antibody against interleukin-1 beta, reduced recurrent cardiovascular events in post-infarction patients with raised hs-CRP without altering lipids, at the cost of more fatal infections.

The distinction decides whether suppression helps or harms. Acute inflammation is largely load-bearing work, and blunting it during the inflammatory phase of wound healing can delay repair; chronic inflammation has no comparable protective role and is a legitimate target.

The reliable error is treating them as one dial. A compound that flattens a cytokine spike in a rodent injected with endotoxin has been tested against an acute six-hour response, and that carries no information about a decade of low-grade inflammation in a human. The reverse mistake also circulates, where a normal standard CRP is offered as proof that no inflammation exists, when the assay used could never measure the range in question.