Table 1.
Studies that have investigated the role of IL-17 family members and IL-23 in sepsis
| Reference | Species | Experimental Design | Main Results |
|---|---|---|---|
| [26] |
M. musculus |
B. fragilis challenge |
Neutralization of IL-17A prevented abscess formation. |
| [23] |
H. sapiens |
Expression analysis in peripheral blood |
Elevation of IL-23(p19) mRNA during sepsis. |
| [27] |
M. musculus |
E. coli challenge |
Neutralization of IL-17A impaired peritoneal clearance of E. coli. |
| [8] |
M. musculus |
CLP |
Neutralization of IL-17A reduced mortality. |
| [22] |
M. musculus |
P. aeruginosa challenge |
Neutralization of IL-23(p19) reduced mortality. |
| [28] |
M. musculus |
CLP |
Production of IL-6, MIP-1α, MIP-2 by cardiomyocytes required endogenous IL-17A. |
| [6] |
M. musculus |
Endotoxemia |
Neutralization of IL-17A or IL-23(p19) improved survival. Regulation of IL-17A and IL-23(p19) by C5a. |
| [9] |
M. musculus |
Endotoxemia, CLP |
C5a dependency of production of IL-17 F. |
| [25] | H. sapiens (premature infants) | Monocytes, DCs | Defect in the production of IL-12/IL-23 p40 in premature infants. |
CLP Cecal ligation and puncture, DCs Dendritic cells.