Objective: Post-stroke infection is a leading cause of acute ischemic stroke mortality. Tryptophan metabolites can modulate the immune response. This study assesses the association between tryptophan metabolism and post-stroke infection.
Methods: Whole blood from the University of Colorado Emergency Medicine Specimen Bank of acute ischemic stroke patients was collected within 72 hours of last known well. Mass spectrometry determined concentrations of tryptophan metabolites. Multivariate logistic regression modeled the association between post-stroke infection within 30 days and metabolite concentrations, controlling for age, sex, NIH stroke scale score, time to sample collection, smoking status, dysphagia, history of chronic kidney or end stage renal disease, and history of diabetes mellitus.
Results: Of 73 subjects, 21 (28.8 %) developed a post-stroke infection. Those with or without a post-stroke infection had similar concentrations of tryptophan, kynurenic acid and quinolinic acid. Those who developed a post-stroke infection had higher mean concentrations of kynurenine (2.3μM, standard deviation 1.1μM) compared to those who did not develop a post-stroke infection (1.6μM , standard deviation 0.6μM, p = 0.01). The adjusted odds ratio of a post-stroke infection within 30 days was 3.94 (95 % Confidence Interval 1.40 - 11.11) for every 1μM increase in kynurenine concentration.
Conclusions: Increasing circulating kynurenine within 72 hours of ischemic stroke onset is associated with increased odds of developing a post-stroke infection within 30 days of emergency department admission. Understanding the causal mechanism of kynurenine promoting post-stroke infection may yield targeted therapeutics that reduce the morbidity and mortality of ischemic stroke.
Keywords: Acute Ischemic stroke; Cerebrovascular infarction; Kynurenine; Stroke; Tryptophan catabolism.
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