| Cell type |
Sepsis-associated response/signaling |
Additional comments: (approach and/or mechanism) |
Reference |
| Peritoneal macrophages from WT and Cav-1 KO mice |
↑ Ability to phagocytize E. coli ↑ LPS-induced: expression of iNOS, production of NO, IL-1β, IL-6, TNF-α, activation of NF-κB |
Reduced expression ofCD14, CD36, TLR4 and MyD88 in Cav-1 KO macrophages |
[38] [70] |
| Neutrophils from WT and Cav-1 KO mice |
↑ Ability to phagocytize P. aeruginosa |
|
[19] |
| Mouse alveolar and peritoneal macrophages |
↓LPS-induced TNF-α and IL-6 production |
siRNA knockdown TLR4-dependent |
[72] [73] |
| Peritoneal macrophages from WT and Cav-1 KO mice |
↓LPS-induced CXCL1, CXCL10, CCL5, TNF-α, IL-6 production |
|
[42] |
| RAW264.7 macrophage cell line |
↓LPS-induced TNF-α and IL-6 production |
Overexpression P38 MAPK-dependent |
[73] |
| B-lymphocytes from WT and Cav-1 KO mice |
↑ LPS-induced IgG3 secretion |
|
[43] |
| Lung endothelial cells from WT and Cav-1 KO mice |
↑ LPS-induced: ICAM-1, TNF-α, iNOS |
Mechanism: Loss of Cav-1 leads to hyperactivation of eNOS resulting in inactivating IRAK4 nitration and impaired TLR4-dependent signaling in Cav-1 KO mice |
[44] |
| Liver sinusoidal endothelial cells from WT and Cav-1 KO mice |
↑ LPS-induced eNOS inhibition |
Cav-1 KO |
[31] |
| Mouse alveolar type 1 (AT-1) cells |
↑ LPS-induced: TNF-α and IL-6 production P38 MAPK and NF-κB activation |
Overexpression |
[40] |