1998
DOI: 10.1023/a:1006891926301
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Abstract: Gram negative sepsis and septic shock continue to be a major medical problem, with a complex physiopathology and it is associated with high mortality. Although secretion of cytokines such as tumor necrosis factor-alpha by macrophages is the principal host mediator of septic shock, other characteristic functions of macrophages implicated in their phagocytic capacity have not been studied in the process of endotoxic shock. In the present study we have used an intraperitoneal injection of E. coli lipopolysacchari… Show more

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Cited by 29 publications
(2 citation statements)
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“…Pro-inflammatory molecules such as NO and TNF-α were examined to evaluate the anti-inflammatory effect of NLE because upon bacterial LPS stimulation, these molecules are known to induce oxidative stress, vascular anomalies such as disseminated intravascular coagulation, vascular perfusion, hypotension, multiple organ failure, and, in severe cases, septic shock and death (MacMicking et al ., 1995; Mayeux, 1997; Víctor et al ., 1998; Yazar et al ., 2010). In order to explore the in vivo effect of NLE, an LPS-induced mouse model of sepsis was established, using specific pathogen-free C57BL/6 mice.…”
Section: Discussionmentioning
confidence: 99%
“…Pro-inflammatory molecules such as NO and TNF-α were examined to evaluate the anti-inflammatory effect of NLE because upon bacterial LPS stimulation, these molecules are known to induce oxidative stress, vascular anomalies such as disseminated intravascular coagulation, vascular perfusion, hypotension, multiple organ failure, and, in severe cases, septic shock and death (MacMicking et al ., 1995; Mayeux, 1997; Víctor et al ., 1998; Yazar et al ., 2010). In order to explore the in vivo effect of NLE, an LPS-induced mouse model of sepsis was established, using specific pathogen-free C57BL/6 mice.…”
Section: Discussionmentioning
confidence: 99%
“…Полученные результаты согласуются с данными литературы [16] и свидетельствуют о снижении продукции лейкоцитами активных форм кислорода, продуцируемых NADPH-оксидазой и миелопероксидазой, а также об угнетении способности к хемотаксису и агрегации при эндотоксиновом шоке [16][17][18]. Такое угнетение функций лейкоцитов при введении ЛПС является следствием чрезмерной активации этих клеток, вследствие прямого контакта рецепторов лейкоцитов с ЛПС, что в конечном итоге приводит к полной дисфункции этих клеток [16,19].…”
Section: при обработке результатов рассчитывали процент падения флуорunclassified