hematopoietic system
N |
• normal myeloid lineage and in vitro M1 and M2 macrophage differentiation
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• decrease in autophagosome formation in response to lipopolysaccharide injection or bacterial infection
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• with TLR stimulation and pan-caspase inhibition treatments
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• decrease in generation of LC3-II by peritonela macrophages following infection with L. monocytogenes indicates impaired induction of autophagy
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immune system
• decrease in autophagosome formation in response to lipopolysaccharide injection or bacterial infection
|
• with TLR stimulation and pan-caspase inhibition treatments
|
• decrease in generation of LC3-II by peritonela macrophages following infection with L. monocytogenes indicates impaired induction of autophagy
|
• elevated levels of Il1 beta and IL18 in LPS stimulated mice suggest hyperactivation of the inflammasome pathway
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• elevated levels of Il1 beta and IL18 in LPS stimulated mice suggest hyperactivation of the inflammasome pathway
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• in cultured macrophages stimulated with LPS and ATP
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• in cultured macrophages stimulated with LPS and ATP
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• along with massive lung tissue destruction upon lipopoysaccharide injection
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homeostasis/metabolism
• elevated levels of Il1 beta and IL18 in LPS stimulated mice suggest hyperactivation of the inflammasome pathway
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• elevated levels of Il1 beta and IL18 in LPS stimulated mice suggest hyperactivation of the inflammasome pathway
|
cellular
• higher in vitro macrophage cell death after lipopolysaccharide injection
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• with TLR stimulation and pan-caspase inhibition treatments
|
• decrease in generation of LC3-II by peritonela macrophages following infection with L. monocytogenes indicates impaired induction of autophagy
|