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Model of sepsis and/or infection with bacterial pathogen	Survival	Inflammatory response	Microvascularpermeabilityin the lung	Bacterial burden(pathogen)	Genetic background	Reference
LPS (i.p.)	↓ ↓ NC	↑ Plasma levels of TNF-α and MIP-1α	↑ LPS-induced Kfc and edema ↑ LPS-induced (Evans Blue)		C57BL/6 x129 C57BL/6 x129? C57BL/6 x129? C57BL/6	[20] [44] [44] [11]
S. Typhimurium(i.v and p.o.)	↑	↓ Serum IL-6, TNF-α, IFN-g		↓ Spleen and liver	C57BL/6	[42]
P. aeruginosastrain 27853 (intratracheal)	↓	↑ BAL IL-1β, MIP-2, TNF-α		↑ Lung	C57BL/6 x129	[84]
P. aeruginosastrains PAO1 or PAK (intranasal)	↑ ↑	↓BAL IL-1β, TNF-α, IL-6 ↓BAL IL-6, TNF-α, and IL-12 ↑ Phagocytic ability of macrophages in vivo		↓ Lung and spleen ↓ Lung, BAL, and serum	C57BL/6 x129 C57BL/6 x129	[19] [80]
E. coli (i.p.)		↑PlasmaIL-1β, TNF-α, IL-6			C57BL/6	[70]
CLP model of sepsis	↑	↓ Serum IL-6, TNF-α ↓Thymocyte apoptosis in vivo	NC Kfc and edema	↓ Spleen and liver	C57BL/6 x129	[16]

Table 2: Positive (?) or negative (?) regulation of major events associated with sepsis by Cav-1 in mice.