Title : Silica-induced chemokine expression in alveolar type II cells is mediated by TNF-alpha-induced oxidant stress.

Pub. Date : 1999 Jun

PMID : 10362723






6 Functional Relationships(s)
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1 Silica-induced chemokine expression in alveolar type II cells is mediated by TNF-alpha-induced oxidant stress. Silicon Dioxide tumor necrosis factor Mus musculus
2 We hypothesize that non-oxidant-mediated silica-cell interactions lead to the upregulation of tumor necrosis factor-alpha (TNF-alpha), whereby TNF-alpha-induced generation of reactive oxygen species (ROS) leads to the activation of the monocyte chemotactic protein (MCP)-1 and macrophage inflammatory protein (MIP)-2 genes. Silicon Dioxide tumor necrosis factor Mus musculus
3 We hypothesize that non-oxidant-mediated silica-cell interactions lead to the upregulation of tumor necrosis factor-alpha (TNF-alpha), whereby TNF-alpha-induced generation of reactive oxygen species (ROS) leads to the activation of the monocyte chemotactic protein (MCP)-1 and macrophage inflammatory protein (MIP)-2 genes. Silicon Dioxide tumor necrosis factor Mus musculus
4 We hypothesize that non-oxidant-mediated silica-cell interactions lead to the upregulation of tumor necrosis factor-alpha (TNF-alpha), whereby TNF-alpha-induced generation of reactive oxygen species (ROS) leads to the activation of the monocyte chemotactic protein (MCP)-1 and macrophage inflammatory protein (MIP)-2 genes. Silicon Dioxide tumor necrosis factor Mus musculus
5 This ROS production could be inhibited with extracellular GSH treatment, and in the case of cristobalite-induced ROS, inhibition was also achieved with an anti-TNF-alpha antibody. Silicon Dioxide tumor necrosis factor Mus musculus
6 The results support the hypothesis that TNF-alpha mediates cristobalite-induced MCP-1 and MIP-2 expression through the generation of ROS. Silicon Dioxide tumor necrosis factor Mus musculus