Targeting the Peripheral Inflammatory Response to Stroke: Role of the Spleen

Pennypacker, Keith R.

doi:10.1007/s12975-014-0372-8

Cited by 28 publications

(17 citation statements)

References 42 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In another retrospective study, the relatively higher level of mononuclear cells in the peripheral blood of ICH patients was closely associated with mortality within 3 months [32]. In an experimental study, removal of the spleen was beneficial in hemorrhagic stroke-induced brain injury by targeting the peripheral inflammatory cells [33], but additional studies are needed to translate these exciting findings into clinical setting.…”

mentioning

confidence: 99%

See 1 more Smart Citation

An Update on Inflammation in the Acute Phase of Intracerebral Hemorrhage

Chen

Yang

Chen

et al. 2014

Transl. Stroke Res.

206

147

View full text Add to dashboard Cite

Intracerebral hemorrhage (ICH) is a common and severe neurological disorder, which is associated with high rates of mortality and morbidity. Despite extensive research into the pathology of ICH, there are still no clinically approved neuroprotective treatments. Currently, increasing evidence has shown that inflammatory responses participate in the pathophysiological processes of brain injury following ICH. In this editorial, we summarized some promising advances in the field of inflammation and ICH, which contained animal and human investigations; discussed the role of neuroinflammation, systemic inflammatory responses, and some potential targets; and focused on the challenges of translation between pre-clinical and clinical studies and potential anti-inflammatory therapeutic approaches after ICH.

show abstract

mentioning

confidence: 99%

“…It is noteworthy that although anti-inflammatory may ameliorate the acute brain injury after ICH, one side effect with this approach is the potentiation of the immune suppression, which results in higher infection rates [33]. Besides, inflammation and immune cells are crucial to the repair and regeneration of brain tissue during the late stage [46][47][48].…”

mentioning

confidence: 99%

An Update on Inflammation in the Acute Phase of Intracerebral Hemorrhage

Chen

Yang

Chen

et al. 2014

Transl. Stroke Res.

206

147

View full text Add to dashboard Cite

show abstract

“…In addition to the release of ROS from activated microglia, these cells also release matrix metalloproteinases that break down the blood-brain barrier (del Zoppo et al, 2007; Shi et al, 2016). Increased blood-brain barrier permeability renders the ischemic hemisphere vulnerable to invading immune cells from the spleen and peripheral immune system (Pennypacker, 2014; Seifert and Pennypacker, 2014). Invading phagocytic cells contribute to oxidative damage in the brain via myeloperoxidase, an enzyme responsible for producing hypochlorous acid, a strong oxidant (Beray-Berthat et al, 2003).…”

Section: 1 Oxidative Stress In Ischemic Strokementioning

confidence: 99%

Targeting antioxidant enzyme expression as a therapeutic strategy for ischemic stroke

Davis

Pennypacker

2017

Neurochemistry International

Self Cite

View full text Add to dashboard Cite

During ischemic stroke, neurons and glia are subjected to damage during the acute and neuroinflammatory phases of injury. Production of reactive oxygen species (ROS) from calcium dysregulation in neural cells and the invasion of activated immune cells are responsible for stroke-induced neurodegeneration. Scientists have failed thus far to identify antioxidant-based drugs that can enhance neural cell survival and improve recovery after stroke. However, several groups have demonstrated success in protecting against stroke by increasing expression of antioxidant enzymes in neural cells. These enzymes, which include but are not limited to enzymes in the glutathione peroxidase, catalase, and superoxide dismutase families, degrade ROS that otherwise damage cellular components such as DNA, proteins, and lipids. Several groups have identified cellular therapies including neural stem cells and human umbilical cord blood cells, which exert neuroprotective and oligoprotective effects through the release of pro-survival factors that activate PI3K/Akt signaling to upregulation of antioxidant enzymes. Other studies demonstrate that treatment with soluble factors released by these cells yield similar changes in enzyme expression after stroke. Treatment with the cytokine leukemia inhibitory factor increases the expression of peroxiredoxin IV and metallothionein III in glia and boosts expression of superoxide dismutase 3 in neurons. Through cell-specific upregulation of these enzymes, LIF and other Akt-inducing factors have the potential to protect multiple cell types against damage from ROS during the early and late phases of ischemic damage.

show abstract

“…However, consequent amplification of the adaptive immune response propels the progress of ischemic brain injury. Immunomodulation (immunotherapy) therefore has become a promising concept for stroke treatment [8–13]. …”

mentioning

confidence: 99%