Inflammation in ischaemic brain injury: current advances and future perspectives.
1. Numerous studies have indicated that inflammation plays a key role in ischaemic brain injury. Brain ischaemia-reperfusion-induced inflammatory responses include increased microglial and astrocyte activity, increased production of cytokines, chemokines, adhesion molecules and metalloproteinases and the infiltration of monocytes and leucocytes into injured brain regions. 2. Although a significant proportion of the inflammatory response appears to exacerbate ischaemic brain injury, certain inflammatory responses are beneficial to ischaemic brains. It is necessary to further identify the detrimental and beneficial inflammatory responses so that therapeutic strategies can be designed for stroke patients to selectively inhibit detrimental responses while enhancing beneficial responses. 3. Increasing evidence also indicates significant changes in the peripheral immune system of stroke patients and animals that undergo cerebral ischaemia. It is worth elucidating the effects of these changes in ischaemic brain damage. 4. There are complex interactions in the ischaemic brain between microglia and other cell types, including neurons, astrocytes, endothelial cells and stem cells. It is of particular interest to determine the mechanisms underlying the roles of high-mobility group box-1, advanced glycation end-products receptors (RAGE), S100B and NADPH oxidase in these interactions. 5. Because brain ischaemia-induced inflammation is a relatively long-lasting event with profound effects on brain injury, it is of considerable importance to further investigate the mechanisms underlying inflammation in ischaemic brains.
Xia
Weiliang
W
Medical-X Research Institute, Shanghai Jiao Tong University, Shanghai, China.
Han
Jin
J
Huang
Gang
G
Ying
Weihai
W
D000818:Animals; D001253:Astrocytes / Q000276:immunology / Q000473:pathology; D002545:Brain Ischemia / Q000276:immunology* / Q000473:pathology; D015815:Cell Adhesion Molecules / Q000502:physiology; D016207:Cytokines / Q000502:physiology; D004660:Encephalitis / Q000276:immunology* / Q000473:pathology; D006609:High Mobility Group Proteins / Q000502:physiology; D006801:Humans; D007962:Leukocytes / Q000276:immunology / Q000473:pathology; D008666:Metalloendopeptidases / Q000502:physiology; D051379:Mice; D017628:Microglia / Q000276:immunology / Q000473:pathology; D009000:Monocytes / Q000276:immunology / Q000473:pathology; D019255:NADPH Oxidases / Q000502:physiology; D009474:Neurons / Q000276:immunology / Q000473:pathology; D051381:Rats; D000067759:Receptor for Advanced Glycation End Products; D011971:Receptors, Immunologic / Q000502:physiology; D020521:Stroke / Q000276:immunology* / Q000473:pathology
D015815:Cell Adhesion Molecules; D016207:Cytokines; D006609:High Mobility Group Proteins; D000067759:Receptor for Advanced Glycation End Products; D011971:Receptors, Immunologic; D019255:NADPH Oxidases; D008666:Metalloendopeptidases