<b>Results:</b> MCAo resulted in profound attenuation of immune activation, as anticipated. t-PA treatment not only worsened neurological deficit, but further reduced lymphocyte and monocyte counts in blood, enhanced plasma levels of both IL-10 and TNFα and decreased various conventional DC subsets in the spleen and cLN, consistent with enhanced immunosuppression and systemic inflammation after stroke.
Altogether these data support BDNF- and IL-10-based mechanisms underlying the neuroprotective potential of SEC therapy for stroke, and further advance the concept of exploiting the pathological link between brain and spleen as therapeutic targets.
We aimed to evaluate the predictive value of three inflammatory biomarkers (interleukin [IL]-9, IL-10, and interferon [IFN]-γ) for stroke and mortality in atrial fibrillation.
We measured baseline IL-6, IL-8, and IL-10 in a case-cohort study of 557 participants with incident stroke over 5.4 years and 951 participants in a cohort sample.
This work was designed to examine the effect of mouse recombinant resistin on mRNA expression of Tumor necrosis factor-α (TNF-α), Interleukin-1β (IL-1β), Interleukin-10 (IL-10), Transforming growth factor-β1 (TGF- β1), and Heat shock protein-70 (HSP-70) in mouse model of stroke.
Subsequent studies identified interleukin-10 as a common regulatory cytokine among all five of the currently recognized Breg cell subsets, several of which can be found in the affected brain hemisphere after induction of experimental stroke in mice.
Stroke triggers a robust and sustained shift in systemic immunity in patients, including specific lymphopenia, robust activation of <i>i</i>NKT cells, systemic production of IL-10, and a prolonged T<sub>H</sub>2-skewed immunity, all are potential contributors to severe immune suppression seen in patients after stroke.
By comparing the serum levels of inflammatory biomarkers, it was observed that IL‑6 and B1R levels tended to decline whereas IL‑10 levels increased in stroke patients from <30 days to over 180 days.
Our findings indicate that IL-10-1082G/A polymorphism may be used as a genetic marker for identifying individuals at increased risk of developing stroke.
IL10-1082 GG genotype was found to significantly predict early stroke progression [OR (95% CI) = 3.72 (1.28-10.76)] and functional outcome by months 1 and 3 [OR (95% CI) = 5.03 (1.15-21.94) and 5.84 (1.07-31.85), respectively], after further corrections for stroke severity and TOAST categories.
Furthermore, intramyocardial injection of wild-type BM-MNCs led to a significant increase in stroke volume (SV) and rate of the development of pressure over time (+dP/dt) compared to hearts injected with either diluent or IL-10 knock-out BM-MNCs.