As in the adult, inflammation appears to mediate and potentiate focal ischemic brain injury in the neonate (38,39). However, certain aspects of the inflammatory response are different in the neonate. For example, neutrophil extravasation from blood vessels, seen after focal ischemia in adult animal models, is not seen in similar models in the neonatal animal (13). In addition, brain vascular permeability and leukocyte recruitment following injections of inflammatory cytokines (Interleukin-ip or tumor necrosis factor-a) into brain are age dependent and higher in three-week-old animals than in newborns or three-month-old animals (40). The role of resident microglia in mediating inflammatory processes is just beginning to be understood in models of neonatal stroke (41). Additionally, the possibility that innate immunity and systemic responses might regulate the brain's inflammatory response is an emerging concept that will greatly affect the understanding of this process (42 ).

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