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Войти в исследования Journal of hepatology · 2010
Brucella-infected hepatocytes mediate potentially tissue-damaging immune responses.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Delpino M Victoria, Barrionuevo Paula, Scian Romina, Fossati Carlos A, Baldi Pablo C
Аннотация
BACKGROUND & AIMS: Hepatic involvement is frequent in human brucellosis. While different histopathological lesions have been reported in these patients, the underlying cellular and molecular mechanisms have not been addressed.
METHODS: This study assessed whether Brucella abortus can infect a human hepatoma cell line and induce a proinflammatory response in these cells.
RESULTS: The bacterium not only infected the human hepatoma cell line HepG2 but also exhibited intracellular replication. The infection induced hepatoma cells to secrete IL-8, and supernatants from Brucella-infected hepatoma cells were shown to induce the migration of human neutrophils. The infection also induced the expression of the intercellular adhesion molecule ICAM-1 on hepatoma cells, and the adhesion of neutrophils to these cells was significantly higher than to uninfected hepatoma cells. ICAM-1 expression was also induced by stimulation of hepatoma cells with supernatants from Brucella-infected neutrophils. While Brucella infection did not induce the expression of matrix metalloproteinases (MMPs) in hepatoma cells, it significantly induced MMP-9 in neutrophils. Hepatoma cell apoptosis was significantly induced by B. abortus infection and also by stimulation with supernatants from Brucella-infected neutrophils.
CONCLUSIONS: The present study provides clues regarding potential mechanisms of tissue damage during liver brucellosis.
METHODS: This study assessed whether Brucella abortus can infect a human hepatoma cell line and induce a proinflammatory response in these cells.
RESULTS: The bacterium not only infected the human hepatoma cell line HepG2 but also exhibited intracellular replication. The infection induced hepatoma cells to secrete IL-8, and supernatants from Brucella-infected hepatoma cells were shown to induce the migration of human neutrophils. The infection also induced the expression of the intercellular adhesion molecule ICAM-1 on hepatoma cells, and the adhesion of neutrophils to these cells was significantly higher than to uninfected hepatoma cells. ICAM-1 expression was also induced by stimulation of hepatoma cells with supernatants from Brucella-infected neutrophils. While Brucella infection did not induce the expression of matrix metalloproteinases (MMPs) in hepatoma cells, it significantly induced MMP-9 in neutrophils. Hepatoma cell apoptosis was significantly induced by B. abortus infection and also by stimulation with supernatants from Brucella-infected neutrophils.
CONCLUSIONS: The present study provides clues regarding potential mechanisms of tissue damage during liver brucellosis.