Abstract
Objective: Stroke-induced immune alterations predispose patients to infections. While the relationship between stroke and the adaptive immune system has been investigated in detail, to date it is unknown whether the innate immune system, which forms the first line of antibacterial defense, is also impaired in stroke patients. We therefore investigated chemotaxis, phagocytosis, oxidative burst, degranulation of defensins, and NETosis in monocytes and in neutrophil granulocytes. Methods: Patients suffering from acute ischemic stroke were recruited within 12 h of symptom onset; blood was sampled on admission and on days 1, 3, 5, and 7. Cell migration, phagocytosis, and oxidative bursting of phagocytes were determined by the MIGRATEST Kit®, the Phagotest Kit®, and the Phagoburst Kit®, respectively. Human neutrophil peptides 1-3 and serum metanephrine levels were measured by enzyme-linked immunosorbent assay, and NETosis was quantified by immunohistochemistry. Results: The key mechanisms required for bacterial killing, oxidative burst and NETosis, were significantly reduced in samples taken from stroke patients whereas migration, phagocytic function, and defensin production remained unimpaired in monocytes and granulocytes from these patients. Interpretation: Stroke-induced immune alterations include impairment of the first-line defense carried out by specialized phagocytes against bacteria. The hypothesis that these alterations enhance susceptibility to acquired infections is supported by our observation that oxidative bursting in monocytes was more impaired in stroke patients with stroke-associated infections.
Published Version
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