Role of DAMPs and of Leukocytes Infiltration in Ischemic Stroke: Insights from Animal Models and Translation to the Human Disease.


Journal

Cellular and molecular neurobiology
ISSN: 1573-6830
Titre abrégé: Cell Mol Neurobiol
Pays: United States
ID NLM: 8200709

Informations de publication

Date de publication:
Apr 2022
Historique:
received: 28 04 2020
accepted: 22 09 2020
pubmed: 1 10 2020
medline: 1 4 2022
entrez: 30 9 2020
Statut: ppublish

Résumé

Stroke is a leading cause of death and disability worldwide. Several mechanisms are involved in the pathogenesis of ischemic stroke (IS). The contributory role of the inflammatory and immunity processes was demonstrated both in vitro and in animal models, and was confirmed in humans. IS evokes an immediate inflammatory response that involves complex cellular and molecular mechanisms. All components of the innate and adaptive immunity systems are involved in several steps of the ischemic cascade. In the early phase, inflammatory and immune mechanisms contribute to the brain tissue damage, whereas, in the late phase, they participate to the tissue repair processes. In particular, damage-associated molecular patterns (DAMPs) appear critical for the promotion of altered blood brain barrier permeability, leukocytes infiltration, tissue edema and brain injury. Conversely, the activation of regulatory T lymphocytes (Tregs) plays protective effects. The identification of specific cellular/molecular elements belonging to the inflammatory and immune responses, contributing to the brain ischemic injury and tissue remodeling, offers the advantage to design adequate therapeutic strategies. In this article, we will present an overview of the knowledge on inflammatory and immunity processes in IS, with a particular focus on the role of DAMPs and leukocytes infiltration. We will discuss evidence obtained in preclinical models of IS and in humans. The main molecular mechanisms useful for the development of novel therapeutic approaches will be highlighted. The translation of experimental findings to the human disease is still a difficult step to pursue. Further investigations are required to fill up the existing gaps.

Identifiants

pubmed: 32996044
doi: 10.1007/s10571-020-00966-4
pii: 10.1007/s10571-020-00966-4
doi:

Types de publication

Journal Article Review

Langues

eng

Sous-ensembles de citation

IM

Pagination

545-556

Informations de copyright

© 2020. Springer Science+Business Media, LLC, part of Springer Nature.

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Auteurs

Rosita Stanzione (R)

IRCCS Neuromed, Pozzilli, IS, Italy. stanzione@neuromed.it.

Maurizio Forte (M)

IRCCS Neuromed, Pozzilli, IS, Italy.

Maria Cotugno (M)

IRCCS Neuromed, Pozzilli, IS, Italy.

Franca Bianchi (F)

IRCCS Neuromed, Pozzilli, IS, Italy.

Simona Marchitti (S)

IRCCS Neuromed, Pozzilli, IS, Italy.

Speranza Rubattu (S)

IRCCS Neuromed, Pozzilli, IS, Italy. rubattu.speranza@neuromed.it.
Department of Clinical and Molecular Medicine, School of Medicine and Psychology, Sapienza University of Rome, Rome, Italy. rubattu.speranza@neuromed.it.

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