Analysis Tools
immune system
|
• the number of macrophages and neutrophils is increased in LPS-treated hearts
• levels of TNF-alpha, IL-6, and IL-1beta are increased in LPS-treated hearts
• mice fed a high-fat diet to induce chronic inflammation show an increase in infiltration of inflammatory monocytes/macrophages into hearts
|
|
• macrophages from LPS-treated hearts show proinflammatory phenotype with higher expression of CCR2 and MHC-II but reduced levels of CD206
• bone marrow derived macrophages (BMDMs) show augmented secretion of inflammatory factors in response to LPS treatment; 31% increase in the levels of proinflammatory CD38 and 24% lower levels of anti-inflammatory CD206, indicating that macrophages are skewed towards a pro-inflammatory phenotype
• however, basal levels of TNF-alpha, IL-1beta, IL-6, and MCP-1 are normal in bone marrow derived macrophages
• treatment of BMDMs with GW3965, a LXR antagonist, prior to LPS stimulation fails to rescue LPS-induced inflammation
|
|
• levels of IL-6 and IL-1beta are increased in LPS-treated hearts
|
|
• LPS-treated mice show increased serum levels of IL-1beta
|
|
• LPS-treated mice show increased serum levels of IL-6
|
|
• level of TNF-alpha is increased in LPS-treated hearts
|
|
• LPS-treated mice show increased serum levels of TNF-alpha
|
|
• mice injected with LPS exhibit an approximate 40% higher mortality rate than wild-type mice, with a median survival of 35 hours compared to 60 hours for wild-type mice
|
cardiovascular system
|
• mice exhibit an increase in aggravated cardiac dysfunction after LPS injection compared to wild-type mice, with a 38% reduction in fractional shortening
• however, mice exhibit normal cardiac function under basal conditions
• treatment of BMDMs with GW3965, a LXR antagonist, prior to LPS stimulation fails to rescue LPS-induced cardiac dysfunction
• mice fed a high-fat diet exhibit worsened cardiac function compared to controls
|
|
• the number of macrophages and neutrophils is increased in LPS-treated hearts
• levels of TNF-alpha, IL-6, and IL-1beta are increased in LPS-treated hearts
• mice fed a high-fat diet to induce chronic inflammation show an increase in infiltration of inflammatory monocytes/macrophages into hearts
|
hematopoietic system
|
• macrophages from LPS-treated hearts show proinflammatory phenotype with higher expression of CCR2 and MHC-II but reduced levels of CD206
• bone marrow derived macrophages (BMDMs) show augmented secretion of inflammatory factors in response to LPS treatment; 31% increase in the levels of proinflammatory CD38 and 24% lower levels of anti-inflammatory CD206, indicating that macrophages are skewed towards a pro-inflammatory phenotype
• however, basal levels of TNF-alpha, IL-1beta, IL-6, and MCP-1 are normal in bone marrow derived macrophages
• treatment of BMDMs with GW3965, a LXR antagonist, prior to LPS stimulation fails to rescue LPS-induced inflammation
|
homeostasis/metabolism
|
• levels of IL-6 and IL-1beta are increased in LPS-treated hearts
|
|
• LPS-treated mice show increased serum levels of IL-1beta
|
|
• LPS-treated mice show increased serum levels of IL-6
|
|
• level of TNF-alpha is increased in LPS-treated hearts
|
|
• LPS-treated mice show increased serum levels of TNF-alpha
|
muscle
|
• mice exhibit an increase in aggravated cardiac dysfunction after LPS injection compared to wild-type mice, with a 38% reduction in fractional shortening
• however, mice exhibit normal cardiac function under basal conditions
• treatment of BMDMs with GW3965, a LXR antagonist, prior to LPS stimulation fails to rescue LPS-induced cardiac dysfunction
• mice fed a high-fat diet exhibit worsened cardiac function compared to controls
|
