Interleukin 10, monocytes and increased risk of early infection in ischaemic stroke

Background and purpose

: The pathophysiology of stroke‐associated infection (SAI) is uncertain. The cytokine profile and peripheral white cell response were assessed in patients with or without SAI.

Methods

The incidence of SAI was assessed in 110 patients with ischaemic stroke allocated antibiotic prophylaxis or placebo within 24?h of clinical onset. Peripheral white cell counts, interleukin (IL)6, tumour necrosis factor (TNF)α and IL10 were measured in plasma.

Results

17 (15%) patients developed infection and showed time‐dependent increases of total white cell count, neutrophils, monocytes, lymphocytes, IL6 and IL10, whereas TNFα and the TNFα/IL10 ratio decreased. In logistic regression, IL10 (odds ratio (OR) 1.08, 95% confidence interval (CI) 1.01 to 1.16), monocyte count (OR 1.42, 95% CI 1.08 to 1.87) and National Institute for Health Stroke Survey score on admission (OR 1.17, 95% CI 1.05 to 1.31) were independent predictors of systemic infection.

Conclusions

SAI is associated with stroke severity, excessive IL10‐mediated response and an increased number of circulating monocytes. These results support the finding that acute ischaemic brain injury triggers a blood‐borne anti‐inflammatory response that decreases the antimicrobial drive of the immune system.Stroke‐associated infection (SAI) has been reported in 21–65% of patients with stroke.^1,2,3,4 A high rate of infection, despite avoidance of invasive manoeuvres³ or prophylactic antibiotics,⁵ suggests that a brain‐mediated immunodepressive state can be an independent contributor to SAI, as recently suggested in a mouse model of transient focal brain ischaemia,⁶ and in patients with brain trauma or neurosurgery.⁷ Several cytokines may increase soon after stroke onset in patients and affect clinical outcome.^8,9 Cytokines are essential mediators in the cross‐talk between the brain and the immune system to maintain homoeostasis,¹⁰ and acute brain injury may facilitate a cytokine‐mediated systemic inflammatory response syndrome, activate neuroimmune pathways, such as the hypothalamic–pituitary–adrenal axis, or the autonomic nervous system,¹¹ and decrease the competence of the immune system.¹² Proinflammatory cytokines released by the injured brain tissue may also transfer to the plasma and set off a compensatory anti‐inflammatory response syndrome that will re‐establish homeostasis only if the degree of proinflammatory and anti‐inflammatory responses is proportionate.¹² Here, our findings support the notion that in patients with acute ischaemic stroke, brain injury may set off a blood‐borne response that decreases the antimicrobial drive of the immune system.