Analysis Tools
immune system
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• primary peritoneal macrophages isolated from mice infected with Mycobacterium tuberculosis (Mtb) strain H37Rv for 24 h show increased intracellular survival of Mtb and accumulate more bacteria than Mtb-infected wild-type macrophages
• macrophages pretreated with the calcium channel blocker bepridil (BPD) and then infected with Mtb show no significant change in intracellular survival of Mtb relative to similarly treated wild-type controls
• macrophages transfected with miR-27a mimic or miR-27a inhibitor and then infected with Mtb for 24 h show no significant changes in bacterial survival of Mtb
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• at 28 days post-infection with Mycobacterium tuberculosis (Mtb) strain H37Rv, mice exhibit a higher granuloma score, increased lymphocyte and neutrophil recruitment, and much higher bacterial titers in lung tissue than Mtb-infected wild-type controls
• mice infected with Mtb for 14 days and then treated with a miR-27a antagomir every 3 days for another 14 days show no significant reduction in the granuloma score or bacterial titers in the lung
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homeostasis/metabolism
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• Mtb-infected primary peritoneal macrophages show a reduced amount of LC3-II and significantly decreased accumulation of LC3 puncta and autophagy flux
• peritoneal macrophages pretreated with chloroquine (CQ) and then infected with Mtb show a decreased LC3-II amount in the presence of CQ
• macrophages pretreated with the calcium channel blocker bepridil (BPD) and then infected with Mtb do not show reduced accumulation of LC3 puncta, unlike similarly treated wild-type macrophages
• at 28 days post-infection with Mtb strain H37Rv, mice show less LC3 immunostaining in lung tissue than Mtb-infected wild-type controls, suggesting that CACNA2D3 may protect mice from Mtb infection by promoting autophagy
• macrophages transfected with miR-27a mimic or miR-27a inhibitor and then infected with Mtb for 24 h show no significant change in the formation of LC3 puncta
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• macrophages infected with Mtb for 1 min show a marked decrease in the intracellular concentration of Ca2+ ions
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cellular
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• Mtb-infected primary peritoneal macrophages show a reduced amount of LC3-II and significantly decreased accumulation of LC3 puncta and autophagy flux
• peritoneal macrophages pretreated with chloroquine (CQ) and then infected with Mtb show a decreased LC3-II amount in the presence of CQ
• macrophages pretreated with the calcium channel blocker bepridil (BPD) and then infected with Mtb do not show reduced accumulation of LC3 puncta, unlike similarly treated wild-type macrophages
• at 28 days post-infection with Mtb strain H37Rv, mice show less LC3 immunostaining in lung tissue than Mtb-infected wild-type controls, suggesting that CACNA2D3 may protect mice from Mtb infection by promoting autophagy
• macrophages transfected with miR-27a mimic or miR-27a inhibitor and then infected with Mtb for 24 h show no significant change in the formation of LC3 puncta
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hematopoietic system
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• primary peritoneal macrophages isolated from mice infected with Mycobacterium tuberculosis (Mtb) strain H37Rv for 24 h show increased intracellular survival of Mtb and accumulate more bacteria than Mtb-infected wild-type macrophages
• macrophages pretreated with the calcium channel blocker bepridil (BPD) and then infected with Mtb show no significant change in intracellular survival of Mtb relative to similarly treated wild-type controls
• macrophages transfected with miR-27a mimic or miR-27a inhibitor and then infected with Mtb for 24 h show no significant changes in bacterial survival of Mtb
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