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Research Highlight

The expanding phenotype of stroke‑induced

immune alterations

Johanna Ruhnau, Antje Vogelgesang, Alexander Dressel
Department of Neurology, Neuroimmunology Section, University Medicine Greifswald, 17489 Greifswald, Germany.

Ruhnau J, Schulze K, Gaida B, Langner S, Kessler C, Broker B, Dressel A, STROKE‑INDUCED IMMUNE ALTERATIONS
Vogelgesang A. Stroke alters respiratory burst in neutrophils and
monocytes. Stroke 2014;45(3):794‑800.
Stroke-induced immune alterations can be observed
in the peripheral blood of stroke patients within the
INTRODUCTION
first hour after stroke. Blood samples obtained shortly
after stroke already exhibit severe lymphocytopenia.
The clinical outcome of ischemic stroke patients is
determined by the extent of the ischemic lesion as Stress hormones are thought to be closely involved
well as the occurrence of severe systemic infections. in these rapid changes; stress hormone levels have
Patients with pneumonia have a three-fold increase in been shown to be elevated in human stroke patients,
30-day mortality, and survivors have poorer clinical blockade of catecholamines prevents SAI in animal
outcomes. [1] models of experimental stroke, and in vitro exposure of
peripheral blood mononuclear cell to stress hormones

Pneumonia has long been known to complicate mimics some aspects of SIIA. [6,7] Our initial observation
the clinical course of many stroke patients. It was in humans that lymphopenia was associated with
assumed that being bedridden and the occurrence susceptibility to infection was subsequently confirmed
of dysphagia would account for the increased risk of by several groups. [3,8]
stroke-associated infections (SAI). However, over the
last years, it has been demonstrated that stroke-induced It was unexpected that these disease induced immune
immune alterations (SIIA) observed in patients and alterations which reduced lymphocyte counts and
experimental stroke models are strong predictors of induced granulocytosis should account for enhanced
subsequent poststroke infections. [2-4] Furthermore, susceptibility to infection because the first line of
one study associated insular stroke localization with defense against these infections is the innate immune
pneumonia. [5] response. In humans, the functional deactivation of
monocytes (e.g. reduced human leukocyte antigen
These findings led to a new concept in which SIIA expression, reduced release of tumor necrosis factor-α)
are causally related to SAI. Here, we briefly outline was detected after cerebral ischemia and was shown to be
the current knowledge on SIIA and SAI and highlight associated with a higher risk of poststroke infections. [3,9]
recent studies that investigated cell functions involved We investigated in detail bactericidal mechanisms of
in early bacterial defense mechanisms. monocytes and granulocytes after stroke.

Granulocytes home to the site of infection and kill
Access this article online pathogens by degranulation and phagocytosis, via a
Quick Response Code: process termed oxidative burst and the release of web-like
Website: structures called neutrophil extracellular traps (NETs).
www.nnjournal.net
During inflammation and infection, granulocytes and
DOI: monocytes are recruited by chemoattractants and
10.4103/2347-8659.135570 inflammatory cytokines. The cells adhere and internalize
pathogens by endocytosis. Due to the generation of toxic

Corresponding Author: Prof. Alexander Dressel, Department of Neurology, University Medicine Greifswald, Sauerbruchstr.,
17489 Greifswald, Germany. E‑mail: adressel@uni‑greifswald.de

Neuroimmunol Neuroinflammation | Volume 1 | Issue 1 | June 2014 15