Purpose of review Inflammation is implicated in ischaemic stroke as a general cardiovascular risk factor, a possible immediate trigger, a component (and possible exacerbating factor) of the response to tissue injury, a marker of future risk, and as a therapeutic target. Each aspect is reviewed. Recent findings Evidence of epidemiological association of inflammatory markers, particularly C-reactive protein, has accrued, but the independence of inflammation from more conventional risk indicators is under question. Other inflammatory markers are associated with intermediate phenotypes such as hypertension. Tissue inflammation in atherosclerotic plaque is of probable relevance in identifying recently symptomatic carotid disease. Both humoral and cellular inflammation are evident following stroke, with evidence that these responses may exacerbate tissue injury. Blockade of interleukin-1, or of neutrophil chemotaxis, has reduced infarct volume in models of stroke but has yet to show benefit in clinical trials. Other anti-inflammatory strategies are promising. Summary Inflammation is implicated in several aspects of acute ischaemic stroke. It remains to be established whether the inflammatory response is a truly independent risk factor in general, or whether specific anti-inflammatory interventions are beneficial either in prevention or acute treatment.