Elevated plasma levels of interleukin-6 (IL-6), a key regulator of the
acute phase response that includes increased fibrinogen synthesis, ha
ve recently been detected in patients with acute stroke. Nevertheless,
the role of the acute phase response in stroke has been controversial
, with some studies suggesting that preexisting infection accounts for
most of the acute phase response. Increased IL-6 could signal the inv
olvement of antiinflammatory activity, since IL-6 stimulates the produ
ction of endogenous antiinflammatory mediators such as interleukin-L r
eceptor antagonist (IL-1RA). To better understand the interaction of p
ro- and antiinflammatory acute phase processes in brain infarction, pl
asma levels of IL-1RA, IL-6, and acute phase proteins including fibrin
ogen and c-reactive protein (CRP) were measured within 4 +/- 2 days of
onset in 50 patients with acute ischemic stroke and in 20 age-matched
healthy controls. After excluding patients with evidence of infection
, both IL-IRA and IL-6 were significantly elevated in stoke patients c
ompared with controls (p < 0.0001). IL-1RA and IL-6 were both signific
antly correlated with levels of CRP, p < 0.05 and p < 0.001, respectiv
ely, but not with each other. Levels of IL-6 and IL-IRA, together with
fibrinogen and CRP were higher in patients with infarcts of greater t
han 3 cm and lowest in patients with lacunar syndromes. Detection of i
ncreased peripheral levels of IL-1RA, IL-6, and additional acute phase
reactants, including CRP, in acute stroke uncomplicated by infection
suggests that an acute phase response to brain infarction occurs and t
hat the magnitude of this response may be related to the volume of inf
arcted brain.