The role of DCs (dendritic cells) as potent
mediators of inflammation has not been sufficiently investigated in
stroke. Therefore, in the present study, circulating mDCPs (myeloid DC precursors),
pDCPs (plasmacytoid DCPs) and tDCPs (total DCPs) were analysed by flow cytometry in (i) healthy controls (n=29), (ii) patients with ACI-S (asymptomatic
cerebral infarction stenosis; n=46), (iii) patients with TIA (transient ischaemic attack; n=39), (iv) patients with AIS (acute
ischaemic stroke; n=73), and (v) patients with AHS (acute haemorrhagic
stroke; n=31). The NIHSS (National Institutes of Health
Stroke Scale) and
infarction size on a CT (computer tomography) scan were evaluated after
stroke. In a patient subgroup, post-mortem immunohistochemical brain analyses were performed to detect mDCs (CD209), pDCs (CD123), T-cells (CD3) and
HLA-DR. In AIS and AHS, the numbers of circulating mDCPs (P<0.005),
pDCPs (P<0.005) and tDCPs (P<0.001) were significantly reduced. A significant inverse correlation was found between the NIHSS and circulating DCPs (P<0.02), as well as between
hsCRP (
high-sensitivity C-reactive protein) and circulating DCPs (P<0.001). Patients with large
stroke sizes on a CT scan had significantly lower numbers of mDCPs (P=0.007),
pDCPs (P=0.05) and tDCPs (P=0.01) than those with smaller
stroke sizes. Follow-up analysis showed a significant recovery of circulating DCPs in the first few days after
stroke. In the infarcted brain, a dense infiltration of mDCs co-localized with T-cells, single pDCs and high
HLA-DR expression were observed. In conclusion,
acute stroke leads to a decrease in circulating DCPs. Potentially, circulating DCPs are recruited from the blood into the infarcted brain and probably trigger cerebral immune reactions there.