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- IRMS - Nicolae Testemitanu SUMPh
- 1. COLECȚIA INSTITUȚIONALĂ
- Congresul consacrat aniversării a 75-a de la fondarea Universității de Stat de Medicină și Farmacie „Nicolae Testemițanu” din Republica Moldova
- Culegere de postere
Please use this identifier to cite or link to this item:
http://hdl.handle.net/20.500.12710/13164
Title: | Immunomodulation after ischemic stroke. Mechanisms and therapeutic implications |
Authors: | Glavan, Danu Gasnaș, Alexandru Groppa, Stanislav |
Keywords: | ischemic stroke;immunity;immunomodulation;inflammation |
Issue Date: | Oct-2020 |
Publisher: | Universitatea de Stat de Medicină şi Farmacie "Nicolae Testemiţanu" |
Abstract: | Introduction
Inflammation of brain tissue after ischemic stroke leads to local and systemic effects.
Immunity suppression by the nervous system results in the protection of nerve tissue from
subsequent inflammatory damage. At the same time, it increases the susceptibility of the
whole body to infections.
Purpose
Description of local and systemic immune changes that
occur after an ischemic stroke, outlining the mechanisms of
immunosuppression induced by cerebral ischemia and the
potential therapeutic implications of these phenomena.
Material and methods
Articles in English were searched on the PubMed Central
and Google Scholar, using the keywords “ischemic stroke”,
“inflammation”, “infection”, “immunomodulation”,
“immunity” and “autoimmunity”. Representative papers
were selected that provided data on pathogenetic pathways
and inflammatory markers in ischemic stroke and their
possible therapeutic approaches.
Results
Inflammatory mechanisms are currently considered as an important target for stroke
therapy. There is evidence that immune signals and mediators can have both detrimental
and beneficial effects in particular stages of the disease process. As an ischemic stroke
occurs, an inflammatory cascade is triggered with cellular elements: neutrophils,
microglia, monocytes/macrophages, T and B lymphocytes and humoral ones: cytokines,
free radicals, damage-associated molecular pattern, autoantibodies, etc. These may be
diagnostic and prognostic factors in ischemic stroke, as well as potential therapeutic
targets for the control of ischemic injury and possible complications.
Currently, the target of immunomodulation translated into clinical trials is focused on
the early phase of toxic neuroinflammation. However, the neuroinflammatory reaction
after acute brain injury continues for months. One of the studied therapies, Fingolimod, a sphingosine-1-phosphate receptor modulator, which
inhibits T lymphocytes, is shown to be promising by
reducing the volume of infarction, the risk of
hemorrhagic transformation and disability in Asians.
There is increasing evidence that dysregulation of the
immune response after the stroke might be an
important predisposing factor for infection.
Conclusions
Evidence suggests that post-ischemic oxidative stress
and inflammation contribute to brain injury and to the
expansion of the ischemic lesion. On the other hand, an
adequate adaptive immune response after acute brain
ischemia also plays an important role in response to
ischemic injury, preventing secondary infarct growth
by counteracting the production of proinflammatory
cytokines and by modulating the activation of
lymphocytes and microglia.
Immunomodulatory therapy seems promising in certain subgroups of patients with
ischemic stroke. By now there are modest data on the benefit of this therapy, collected
from small populations, further studies which will help us select these subgroups being
needed. |
URI: | https://stiinta.usmf.md/ro/manifestari-stiintifice/zilele-universitatii http://repository.usmf.md/handle/20.500.12710/13164 |
Appears in Collections: | Culegere de postere
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