ABSTRACT
Atherosclerosis is an inflammatory disease, and ischemic stroke is one of its most common and devastating manifestations. Proinflammatory cytokines play a key role in the progression of the irreversible ischemic lesions. The presence of anti-inflammatory mediators may prevent secondary ischemic injury. Objectives 1) To assess the relationship between stroke severity and the serum levels of IL-1β, IL-2, and IL-10; and 2) To analyze the neurological outcome after 72 h of ischemic stroke onset and expression of interleukins. Method We measured the serum levels of IL-1β, IL-2, and IL-10 in 26 patients with acute stroke. Neurological impairment was scored using the National Institute of Health Stroke Scale within the first 72 h after stroke onset. Thirty healthy subjects were analyzed as controls. Results Patients with IL-10 <925.0 pg/mL presented with neurological deterioration within the first 72 h. Conclusion IL-10 may protect against ischemic injury during the acute phase of stroke. .
Aterosclerose é considerada um doença inflamatória e o acidente vascular cerebral (AVC) isquêmico uma de suas principais manifestações. Citocinas pró-inflamatórias exercem importante função na progressão para uma lesão isquêmica irreversível. A presença de mediadores anti-inflamatórios age prevenindo a lesão isquêmica secundária. Objetivos 1) Avaliar a relação entre gravidade do AVC e níveis de IL-1β, IL-2 e IL-10; 2) Avaliar a relação entre prognóstico neurológico nas primeiras 72 horas do AVC e o nível destas citocinas. Método Mensuramos os níveis de IL-1β, IL-2 e IL-10 de 26 pacientes com AVC isquêmico. O comprometimento neurológico foi avaliado através da escala do National Institute of Health nas primeiras 72 horas do AVC. Trinta indivíduos saudáveis foram usados como controles. Resultados Pacientes com IL-10 <925,0 pg/mL apresentaram deterioração neurológica nas primeiras 72 horas após o início do AVC. Conclusão IL-10 pode apresentar um efeito protetor contra a progresso da lesão isquêmica durante a fase aguda do AVC. .
Subject(s)
Adult , Aged , Aged, 80 and over , Female , Humans , Male , Middle Aged , Brain Ischemia/prevention & control , Interleukin-1beta/blood , /blood , /blood , Intracranial Arteriosclerosis/blood , Stroke/blood , Case-Control Studies , Disease Progression , Enzyme-Linked Immunosorbent Assay , Intracranial Arteriosclerosis/complications , Prognosis , Risk Factors , Severity of Illness Index , Statistics, Nonparametric , Stroke/etiology , Time FactorsABSTRACT
UNLABELLED: Atherosclerosis is an inflammatory disease, and ischemic stroke is one of its most common and devastating manifestations. Proinflammatory cytokines play a key role in the progression of the irreversible ischemic lesions. The presence of anti-inflammatory mediators may prevent secondary ischemic injury. OBJECTIVES: 1) To assess the relationship between stroke severity and the serum levels of IL-1ß, IL-2, and IL-10; and 2) To analyze the neurological outcome after 72 h of ischemic stroke onset and expression of interleukins. METHOD: We measured the serum levels of IL-1ß, IL-2, and IL-10 in 26 patients with acute stroke. Neurological impairment was scored using the National Institute of Health Stroke Scale within the first 72 h after stroke onset. Thirty healthy subjects were analyzed as controls. RESULTS: Patients with IL-10 <925.0 pg/mL presented with neurological deterioration within the first 72 h. CONCLUSION: IL-10 may protect against ischemic injury during the acute phase of stroke.
Subject(s)
Brain Ischemia/prevention & control , Interleukin-10/blood , Interleukin-1beta/blood , Interleukin-2/blood , Intracranial Arteriosclerosis/blood , Stroke/blood , Adult , Aged , Aged, 80 and over , Case-Control Studies , Disease Progression , Enzyme-Linked Immunosorbent Assay , Female , Humans , Intracranial Arteriosclerosis/complications , Male , Middle Aged , Prognosis , Risk Factors , Severity of Illness Index , Statistics, Nonparametric , Stroke/etiology , Time FactorsABSTRACT
Interferon-beta (IFN-beta) is of benefit in the treatment of multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE), but the mechanisms by which it exerts this beneficial effect remain uncertain. The present data demonstrate that IFN-beta therapy impairs the proliferative response to concanavalin A (ConA) and myelin basic protein (MBP), decreases expression of the CD80 molecule on leukocytes of treated mice, and may thereby impede the Th1 cell activation-promoting anergy in EAE. Moreover, IFN-beta therapy increases expression of the CTLA4 molecule, which induces a counterregulatory Th2 response. The reduction of CD80 expression with concomitant increase of CTLA4 expression alters the course of EAE and may be useful as a monitor in therapy with IFN-beta.