RESUMO
Anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis is a type of newly recognized autoimmune encephalitis which is commonly seen in children, but its precise etiology is still uncertain. To reveal the etiology of anti-NMDAR encephalitis is very necessary for understanding its pathology, and for starting immune-related therapy as early as possible to improve its prognosis. In the initial literature, tumor, especially teratoma is more related with the anti-NMDAR encephalitis. In recent research, its etiology is related to infection and heredity. This article reviews the recognition and variation of the etiology of anti-NMDAR encephalitis.
Assuntos
Encefalite Antirreceptor de N-Metil-D-Aspartato/etiologia , Encefalite Antirreceptor de N-Metil-D-Aspartato/genética , Humanos , Infecções/complicaçõesRESUMO
Maternal infection during pregnancy is associated with an increased risk of neurodevelopmental injury. Our aim was to investigate whether prenatal immune challenge could alter susceptibility to seizure-induced brain injury in adulthood. Pregnant Wistar rats were injected intraperitoneally with lipopolysaccharide (LPS) or normal saline (NS) at days 15 and 16 of gestation. At postnatal day 45, seizure susceptibility was assessed in response to lithium-pilocarpine (LiPC) in adult offspring. Four groups were studied, including normal control (NS-NS), prenatal inflammation (LPS-NS), adult seizure (NS-LiPC), and "two-hit" (LPS-LiPC) groups. Our results demonstrated that adult rat offspring of LPS-exposed dams showed significantly greater susceptibility to LiPC-induced seizures, as well as enhanced hippocampal neuronal injury after seizures. Furthermore, animals in the "two-hit" group performed significantly worse than those from the NS-LiPC group in the open field test and Morris water maze. Our findings suggest that prenatal immune activation can cause a long-lasting increase in seizure susceptibility and predispose the brain to the damaging effect of seizures later in life.
Assuntos
Lesões Encefálicas/etiologia , Suscetibilidade a Doenças/complicações , Efeitos Tardios da Exposição Pré-Natal/fisiopatologia , Convulsões/complicações , Convulsões/etiologia , Fatores Etários , Animais , Animais Recém-Nascidos , Lesões Encefálicas/patologia , Modelos Animais de Doenças , Comportamento Exploratório/efeitos dos fármacos , Feminino , Hipocampo/efeitos dos fármacos , Hipocampo/patologia , Deficiências da Aprendizagem/etiologia , Lipopolissacarídeos/toxicidade , Cloreto de Lítio/toxicidade , Masculino , Aprendizagem em Labirinto/efeitos dos fármacos , Agonistas Muscarínicos/toxicidade , Pilocarpina/toxicidade , Gravidez , Ratos , Ratos Wistar , Convulsões/patologia , Fatores de TempoRESUMO
Our aim was to examine whether neonatal lipopolysaccharide (LPS) exposure is associated with changes in microglia and whether these alternations could influence later seizure-induced neurobehavioral outcomes. Male pups were first injected intraperitoneally with either LPS or saline on postnatal day 3 (P3) and postnatal day 5 (P5). Immunohistochemical analysis showed that LPS-treated animals exhibited increased microglia activation that persisted into adolescence. At P45, seizures were induced in rats by intraperitoneal injection of kainic acid (KA). Rats treated with LPS neonatally showed significantly greater proinflammatory responses and performed significantly worse in the Y-maze, Morris water maze, and inhibitory avoidance tasks after KA insult. Treatment with minocycline at the time of neonatal LPS exposure to block LPS-induced microglia alternation attenuated the exaggerated neuroinflammatory responses and alleviated memory impairment associated with the KA insult. Our findings suggest that neonatal immune activation can predispose the brain to exacerbated behavioral deficits following seizures in adulthood, possibly by priming microglia.
