The possible contribution of microglia and macrophages to delayed neuronal death after ischemia.
Macrophages have long been known to be involved in cytotoxic actions in many tissues in the body following infection. Knowledge of the post-injury actions of blood-borne macrophages in the brain, and their resident counterparts, the microglia, have been limited to the "mopping-up" of cellular debris. However, other functions are now coming to light and there is evidence that they contribute to both growth promotion and cytotoxicity following injury in the brain. This review raises the possibility that macrophages may contribute to delayed neuronal death following ischemia. Growth factors including certain cytokines produced by these cells protect against ischemia-induced neuronal death. In contrast, cytokines can also induce macrophages to synthesize nitric oxide synthase and indoleamine-2,3-dioxygenase which results in the production of the cytotoxins nitric oxide and quinolinic acid. It is hypothesized that viable cells produce or concentrate growth factors which prevent the induction of these enzymes, whereas damaged cells cannot.
Lees
G J
GJ
Department of Psychiatry and Behavioural Science, School of Medicine, University of Auckland, New Zealand.
D000818:Animals; D002545:Brain Ischemia / Q000473:pathology* / Q000503:physiopathology; D016923:Cell Death; D016207:Cytokines / Q000502:physiology; D006133:Growth Substances / Q000502:physiology; D006801:Humans; D002546:Ischemic Attack, Transient / Q000473:pathology / Q000503:physiopathology; D008264:Macrophages / Q000502:physiology*; D008648:Mesoderm / Q000502:physiology; D009474:Neurons / Q000473:pathology*
D016207:Cytokines; D006133:Growth Substances