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Aging and Disease    2014, Vol. 5 Issue (5) : 327-339     DOI: 10.14336/AD.2014.0500327
Catecholamines, Steroids and Immune Alterations in Ischemic Stroke and Other Acute Diseases
Juliane Schulze, Antje Vogelgesang, Alexander Dressel
Section of Neuroimmunology, Department of Neurology, University Medicine Greifswald, Germany
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The outcome of stroke patients is not only determined by the extent and localization of the ischemic lesion, but also by stroke-associated infections. Stroke-induced immune alterations, which are related to stroke-associated infections, have been described over the last decade. Here we review the evidence that catecholamines and steroids induced by stroke result in stroke-induced immune alterations. In addition, we compare the immune alterations observed in other acute diseases such as myocardial infarction, brain trauma, and surgical trauma with the changes seen in stroke-induced immune alterations.

Keywords ischemic stroke      immune      aging      catecholamines      steroids     
Corresponding Authors: Alexander Dressel   
Issue Date: 12 November 2014
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Juliane Schulze
Antje Vogelgesang
Alexander Dressel
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Juliane Schulze,Antje Vogelgesang,Alexander Dressel. Catecholamines, Steroids and Immune Alterations in Ischemic Stroke and Other Acute Diseases[J]. Aging and Disease, 2014, 5(5): 327-339.
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Most innate immune cellsBoth αAR and βAR families
Bone marrow-derived dendritic cellsα1AR α2AR
β1AR β2AR
α1AR α2AR
Natural killer cellsβ2AR
Resting and activated B cells
Naïve T cells and Th1 cells, but not Th2 cells
Regulatory T cells and Th17 cellsNo data available
Table 1.  Expression of adrenoreceptors on immune cells.

induce apoptosis in immature DCs [29]

reduction of MHCII, costimulatory molecules and cytokine expression [30, 31]

inhibition of migration in vivo and in vitro [32]; [33] by downregulation of CCR7 [34]

induction of a tolerogenic DC phenotype that induces T cell anergy, suppression of T cells and generates Tregs [35]

enhanced surface expression of MHCII, CD80 and CD86 [36]

control cell migration via α1bAR [37] and induction of an anti-inflammatory cytokine profile [38]

enhancement of IL-33 production thus promoting Th2 responses [39] inhibited the lipopolysaccharide (LPS)-stimulated production of interleukin (IL)-23, IL-12 p40, tumor necrosis factor (TNF)-alpha and IL-6 [40]


suppressed activation by IL-10 induction and inhibition of upregulation of pro-inflammatory CD163 [41]

development of myeloid suppressor cell like phenotype [42]

cAMP/PKA dependent stimulation of IL-10 promoter/enhancer [43]

upregulate L-selectin in vitro [44]

inhibit IL-6 secretion via αAR [45] but

induce secretion of IL-6 (in the presence of GC) via βAR [46]


suppression of adhesion molecule expression inhibits rolling, adhesion and transmigration [47]

increase of BM-derived neutrophils in blood [48]

promotes necrosis [49]

increase the total circulating neutrophil pool for a few hours [50]

increase expression and release of Hsp72 [51]

suppression of CD11b and inhibition of suppression of CD62L (L-selectin) [52]

decreased phagocytosis of zymosan in vitro [53]

B cells

reduction of splenic and LN B cell numbers

inhibit B cell progenitor proliferation

enhance IgE, suppressed IgG production [54, 55]

state of B cell activation decisive about effect of CA:

- enhanced IgG1 production and IgE on NE exposure during antigen processing or after Th2 coculture [56]

- increase in costimulatory capacity (CD86 upregulation) [57]

- β2AR engagement in presence of IL-4 enhances IgE [58]

T cells

affect thymocyte maturation by inducing apoptosis in thymocytes; more sensitive than Teff than Treg cells [59, 60]

physiological doses: shift from Th1 response to Th2 [61]

pharmacological doses induce anti-inflammation:

- reduce RORγt in Th17 cells [62]

- inhibit TH1 function by direct inhibition of STAT4 and T-bet [63, 64]

- suppress STAT6 function in Th2 by interfering with GATA [65, 66]

β2AR engagement enhances IFNγ production in TH1 cells the presence of IL-12 in pre activated TH1 cells [67]

inhibit IFN-γ in resting TH1 cells [13]

NK cells

impair NK cell function via histone deacetylation and transrepression [68]

inhibit NK cytotoxic functions by:

- reduced TNF-α, IFN-γ, and GM-CSF

- impaired, target binding [69]

Table 2.  Cellular effects of stress hormones in immune cells
Figure 1.  Systemic effects of the stress response in ischemic stroke. The scheme depicts those organ specific immune alterations that occur in stroke and have been experimentally linked to the activation of either the HPA axis or the sympathetic nervous system. As a result the stress response reduces the ability to fight bacteria and increases the risk of subsequent infection. (HPA, hypothalamic-pituitary gland-adrenal; iNKT, invariant natural killer T cells; IFN-g, Interferon-gamma; IL-10, Interleukin-10; TNF-a, tumor necrosis factor-alpha; ↑, increase, ↓, decrease)
Ischemic stroke (IS)Traumatic brain injury (TBI)Myocardial infarction (MI)(Surgical) trauma (ST/T)
innate immune system
White blood cell[98, 100][101][102][98, 103]
monocytic HLA-DR[98, 100, 104][98][105, 106][106, 107]
monocytic LPS activatability[98, 104][98][108]
IL-10[104, 109][110][94][43][111]
IL-6[98, 109][110][101, 113][98, 102][112][111]
HMGB-1[76, 99][114][99][95, 115]
adaptive immune system
circulatory lymphocyte number[77][7, 100, 109, 116, 117][113][98][105, 106][107]
T lymphocyte activation[116][76][118]
IgG, IgM[117][119, 120]
T-cell proliferation to mitogen[117] [76][113]
catecholamines[77][4, 75, 76, 109][94][96, 97][95]
cortisol/corticosterone[77][100, 104][98][106]
Table 3.  Immune alterations immediately after disease onset.
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