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Post-ischemic inflammation in the brain.

Shichita T, Sakaguchi R, Suzuki M, Yoshimura A - Front Immunol (2012)

Bottom Line: Post-ischemic inflammation is an essential step in the progression of brain ischemia-reperfusion injury.Brain ischemia is a sterile organ, but injury-induced inflammation is mostly dependent on Toll-like receptor (TLR) 2 and TLR4.Some endogenous TLR ligands, high mobility group box 1 (HMGB1) and peroxiredoxin family proteins, in particular, are implicated in the activation and inflammatory cytokine expression in infiltrating macrophages.

View Article: PubMed Central - PubMed

Affiliation: Department of Microbiology and Immunology, School of Medicine, Keio University Tokyo, Japan.

ABSTRACT
Post-ischemic inflammation is an essential step in the progression of brain ischemia-reperfusion injury. In this review, we focus on the post-ischemic inflammation triggered by infiltrating immune cells, macrophages, and T lymphocytes. Brain ischemia is a sterile organ, but injury-induced inflammation is mostly dependent on Toll-like receptor (TLR) 2 and TLR4. Some endogenous TLR ligands, high mobility group box 1 (HMGB1) and peroxiredoxin family proteins, in particular, are implicated in the activation and inflammatory cytokine expression in infiltrating macrophages. Following macrophage activation, T lymphocytes infiltrate the ischemic brain and regulate the delayed phase inflammation. IL-17-producing γδT lymphocytes induced by IL-23 from macrophages promote ischemic brain injury, whereas regulatory T lymphocytes suppress the function of inflammatory mediators. A deeper understanding of the inflammatory mechanisms of infiltrating immune cells may lead to the development of novel neuroprotective therapies.

No MeSH data available.


Related in: MedlinePlus

Post-ischemic inflammation in the brain. Within 24 h after ischemic stroke onset, various inflammatory mediators are expressed in ischemic brain tissue. ICAM-1 promotes leukocytes infiltration. Cytokines activate infiltrating leukocytes and directly induce ischemic injury in brain cells. Matrix metalloproteinases (MMPs) alter the permeability of epithelial cells and are implicated in BBB breakdown. Endogenous TLR ligands (DAMPs) are released from necrotic brain cells and activate infiltrating immune cells. These inflammatory mediators trigger post-ischemic inflammation by infiltrating leukocytes. There are currently few effective therapies for this phase of leukocyte infiltration.
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Figure 1: Post-ischemic inflammation in the brain. Within 24 h after ischemic stroke onset, various inflammatory mediators are expressed in ischemic brain tissue. ICAM-1 promotes leukocytes infiltration. Cytokines activate infiltrating leukocytes and directly induce ischemic injury in brain cells. Matrix metalloproteinases (MMPs) alter the permeability of epithelial cells and are implicated in BBB breakdown. Endogenous TLR ligands (DAMPs) are released from necrotic brain cells and activate infiltrating immune cells. These inflammatory mediators trigger post-ischemic inflammation by infiltrating leukocytes. There are currently few effective therapies for this phase of leukocyte infiltration.

Mentions: Brain cells, including astrocytes, oligodendrocytes, endothelium, and pericytes, constitute a neurovascular network, which is essential for metabolic requirement of neurons (Iadecola, 2004; Fraser, 2011). These brain cells also contribute to triggering post-ischemic inflammation by producing inflammatory mediators. TNF-α, IL-1β, NOS (nitric oxide synthetase), and MMPs which enhance cerebrovascular permeability and exaggerate brain edema (Takano et al., 2009; Morancho et al., 2010). Thus, Infiltrating leukocytes and injured brain cells produce various inflammatory mediators, leading to the beginning of post-ischemic inflammation (Barone and Feuerstein, 1999; Figure 1).


Post-ischemic inflammation in the brain.

Shichita T, Sakaguchi R, Suzuki M, Yoshimura A - Front Immunol (2012)

Post-ischemic inflammation in the brain. Within 24 h after ischemic stroke onset, various inflammatory mediators are expressed in ischemic brain tissue. ICAM-1 promotes leukocytes infiltration. Cytokines activate infiltrating leukocytes and directly induce ischemic injury in brain cells. Matrix metalloproteinases (MMPs) alter the permeability of epithelial cells and are implicated in BBB breakdown. Endogenous TLR ligands (DAMPs) are released from necrotic brain cells and activate infiltrating immune cells. These inflammatory mediators trigger post-ischemic inflammation by infiltrating leukocytes. There are currently few effective therapies for this phase of leukocyte infiltration.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3400935&req=5

Figure 1: Post-ischemic inflammation in the brain. Within 24 h after ischemic stroke onset, various inflammatory mediators are expressed in ischemic brain tissue. ICAM-1 promotes leukocytes infiltration. Cytokines activate infiltrating leukocytes and directly induce ischemic injury in brain cells. Matrix metalloproteinases (MMPs) alter the permeability of epithelial cells and are implicated in BBB breakdown. Endogenous TLR ligands (DAMPs) are released from necrotic brain cells and activate infiltrating immune cells. These inflammatory mediators trigger post-ischemic inflammation by infiltrating leukocytes. There are currently few effective therapies for this phase of leukocyte infiltration.
Mentions: Brain cells, including astrocytes, oligodendrocytes, endothelium, and pericytes, constitute a neurovascular network, which is essential for metabolic requirement of neurons (Iadecola, 2004; Fraser, 2011). These brain cells also contribute to triggering post-ischemic inflammation by producing inflammatory mediators. TNF-α, IL-1β, NOS (nitric oxide synthetase), and MMPs which enhance cerebrovascular permeability and exaggerate brain edema (Takano et al., 2009; Morancho et al., 2010). Thus, Infiltrating leukocytes and injured brain cells produce various inflammatory mediators, leading to the beginning of post-ischemic inflammation (Barone and Feuerstein, 1999; Figure 1).

Bottom Line: Post-ischemic inflammation is an essential step in the progression of brain ischemia-reperfusion injury.Brain ischemia is a sterile organ, but injury-induced inflammation is mostly dependent on Toll-like receptor (TLR) 2 and TLR4.Some endogenous TLR ligands, high mobility group box 1 (HMGB1) and peroxiredoxin family proteins, in particular, are implicated in the activation and inflammatory cytokine expression in infiltrating macrophages.

View Article: PubMed Central - PubMed

Affiliation: Department of Microbiology and Immunology, School of Medicine, Keio University Tokyo, Japan.

ABSTRACT
Post-ischemic inflammation is an essential step in the progression of brain ischemia-reperfusion injury. In this review, we focus on the post-ischemic inflammation triggered by infiltrating immune cells, macrophages, and T lymphocytes. Brain ischemia is a sterile organ, but injury-induced inflammation is mostly dependent on Toll-like receptor (TLR) 2 and TLR4. Some endogenous TLR ligands, high mobility group box 1 (HMGB1) and peroxiredoxin family proteins, in particular, are implicated in the activation and inflammatory cytokine expression in infiltrating macrophages. Following macrophage activation, T lymphocytes infiltrate the ischemic brain and regulate the delayed phase inflammation. IL-17-producing γδT lymphocytes induced by IL-23 from macrophages promote ischemic brain injury, whereas regulatory T lymphocytes suppress the function of inflammatory mediators. A deeper understanding of the inflammatory mechanisms of infiltrating immune cells may lead to the development of novel neuroprotective therapies.

No MeSH data available.


Related in: MedlinePlus