krn-7000 and Brain-Ischemia

krn-7000 has been researched along with Brain-Ischemia* in 2 studies

Other Studies

2 other study(ies) available for krn-7000 and Brain-Ischemia

Article	Year
Infiltration of invariant natural killer T cells occur and accelerate brain infarction in permanent ischemic stroke in mice. Neuroscience letters, 2016, 10-28, Volume: 633 Invariant natural killer T (iNKT) cells are a unique subset of T cells that have been implicated in inflammation, atopy, autoimmunity, infections, and cancer. Although iNKT cells have been extensively studied over the past decade, its role in the pathogenesis of ischemic brain injury is still largely unknown. In our study, we determined whether iNKT cells infiltration occur in a mouse model of permanent cerebral ischemia. C57BL6/J male mice were treated with either alpha-galactosylceramide (α-GalCer) or vehicle control before undergoing permanent middle cerebral artery occlusion (pMCAO). α-GalCer, a glycolipid antigen, specifically activates iNKT cells by a CD1d-restricted mechanism. Using flow cytometry, 10,000 leukocytes (CD45 high cells) from the ischemic hemisphere and peripheral blood respectively were analyzed to determine the number of NK1.1 Topics: Animals; Brain; Brain Edema; Brain Infarction; Brain Ischemia; Cytokines; Cytotoxicity, Immunologic; Galactosylceramides; Infarction, Middle Cerebral Artery; Killer Cells, Natural; Lymphocyte Activation; Male; Mice, Inbred C57BL	2016
Functional innervation of hepatic iNKT cells is immunosuppressive following stroke. Science (New York, N.Y.), 2011, Oct-07, Volume: 334, Issue:6052 Systemic immunosuppression has been associated with stroke for many years, but the underlying mechanisms are poorly understood. In this study, we demonstrated that stroke induced profound behavioral changes in hepatic invariant NKT (iNKT) cells in mice. Unexpectedly, these effects were mediated by a noradrenergic neurotransmitter rather than a CD1d ligand or other well-characterized danger signals. Blockade of this innervation was protective in wild-type mice after stroke but had no effect in mice deficient in iNKT cells. Selective immunomodulation of iNKT cells with a specific activator (α-galactosylceramide) promoted proinflammatory cytokine production and prevented infections after stroke. Our results therefore identify a molecular mechanism that leads to immunosuppression after stroke and suggest an attractive potential therapeutic alternative to antibiotics, namely, immunomodulation of iNKT cells to prevent stroke-associated infections. Topics: Adrenergic Agents; Animals; Anti-Bacterial Agents; Bacterial Infections; Brain Ischemia; Cell Movement; Cytokines; Galactosylceramides; Immune Tolerance; Immunomodulation; Infarction, Middle Cerebral Artery; Liver; Lymphocyte Activation; Mice; Mice, Inbred BALB C; Microvessels; Natural Killer T-Cells; Norepinephrine; Propranolol	2011

Article

Year

Infiltration of invariant natural killer T cells occur and accelerate brain infarction in permanent ischemic stroke in mice.

Neuroscience letters, 2016, 10-28, Volume: 633

Invariant natural killer T (iNKT) cells are a unique subset of T cells that have been implicated in inflammation, atopy, autoimmunity, infections, and cancer. Although iNKT cells have been extensively studied over the past decade, its role in the pathogenesis of ischemic brain injury is still largely unknown. In our study, we determined whether iNKT cells infiltration occur in a mouse model of permanent cerebral ischemia. C57BL6/J male mice were treated with either alpha-galactosylceramide (α-GalCer) or vehicle control before undergoing permanent middle cerebral artery occlusion (pMCAO). α-GalCer, a glycolipid antigen, specifically activates iNKT cells by a CD1d-restricted mechanism. Using flow cytometry, 10,000 leukocytes (CD45 high cells) from the ischemic hemisphere and peripheral blood respectively were analyzed to determine the number of NK1.1

Topics: Animals; Brain; Brain Edema; Brain Infarction; Brain Ischemia; Cytokines; Cytotoxicity, Immunologic; Galactosylceramides; Infarction, Middle Cerebral Artery; Killer Cells, Natural; Lymphocyte Activation; Male; Mice, Inbred C57BL

2016

Functional innervation of hepatic iNKT cells is immunosuppressive following stroke.

Science (New York, N.Y.), 2011, Oct-07, Volume: 334, Issue:6052

Systemic immunosuppression has been associated with stroke for many years, but the underlying mechanisms are poorly understood. In this study, we demonstrated that stroke induced profound behavioral changes in hepatic invariant NKT (iNKT) cells in mice. Unexpectedly, these effects were mediated by a noradrenergic neurotransmitter rather than a CD1d ligand or other well-characterized danger signals. Blockade of this innervation was protective in wild-type mice after stroke but had no effect in mice deficient in iNKT cells. Selective immunomodulation of iNKT cells with a specific activator (α-galactosylceramide) promoted proinflammatory cytokine production and prevented infections after stroke. Our results therefore identify a molecular mechanism that leads to immunosuppression after stroke and suggest an attractive potential therapeutic alternative to antibiotics, namely, immunomodulation of iNKT cells to prevent stroke-associated infections.

Topics: Adrenergic Agents; Animals; Anti-Bacterial Agents; Bacterial Infections; Brain Ischemia; Cell Movement; Cytokines; Galactosylceramides; Immune Tolerance; Immunomodulation; Infarction, Middle Cerebral Artery; Liver; Lymphocyte Activation; Mice; Mice, Inbred BALB C; Microvessels; Natural Killer T-Cells; Norepinephrine; Propranolol

2011