|
| Authors/year | Sepsis model | MSC type/combination | Biological effect | Clinical effect | Source ref. |
|
| Asano et al. (2015) | TSS SEA + LPS mouse model | A-MSC (1 × 106) | ↓ INF-γ, TNF-α, IL-6, IL-2
= Treg, IL-10 | ↓ 40 h mortality | [25] |
| Kim et al. (2014) | TSS SEB mouse model | hMSC, mMSC (2 × 105) | ↓ TNF-α, IL-2, IL-6 | = mortality
No difference between hMSC and mMSC | [26] |
| Ou et al. (2016) | LPS mouse model | A-MSC, BM-MSC | ↓ IL-8 (A-MSC)
↓ proinflammatory cytokines (both types) | ↓ mortality | [27] |
| Pedrazza et al. (2014) | E. coli-induced peritonitis | A-MSC (1 × 106) | ↓ IL-6, MCP-1
↓ AST, ALT
↓ splenocyte apoptosis | ↓ 26 h mortality | [28] |
| Chao et al. (2014) | CLP-polymicrobial mouse model | BM-MSC
UC-MSC
(5 × 106) | ↓ IL-6 and TNF-α
↑ CD3+CD4+CD25+ Treg | ↓ 7- and 14-day mortality | [29] |
| Alcayaga-Miranda et al. (2015) | CLP-polymicrobial mouse model | Men-MSC, A-MSC, BM-MSC (2 × 106)/enrofloxacin | In vitro: ↑ inhibition of bacterial growth (Men-MSC)
No difference—Men-MSC versus A-MSC/BM-MSC in the dynamics of cytokines | Men-MSC + ATB
↓ 96 h mortality | [30] |
| Wang et al. (2015) | CLP-polymicrobial mouse model | D-MSC (2 × 106) | ↓ IL-1, IL-6
↑ IL-4, IL-5
IL-10 without significant changes
In vitro: inhibition of macrophage apoptosis, increased migration intensity | ↓ 10-day mortality | [31] |
| Liu et al. (2016) | CLP-polymicrobial mouse model | Unspecified (1 × 106) | ↓ NK
↓ TNF-α, IL-6, INF-γ
↑ IL-10 | ↓ 72 h mortality | [35] |
| Sepúlveda et al. (2014) | LPS mouse model | BM-MSC (1 × 105) | In vitro: no difference between senescent versus immortalised
In vivo: no reduction of proinflammatory cytokine levels in senescent cells | Immortalised MSC: ↓ 24, 48, 72, 96, 120, and 144 h mortality versus senescent type | [36] |
| Wu et al. (2016) | CLP-polymicrobial sepsis | UC-MSC | ↓ TNF-α, MCP-1, IL1, 6
↑ IL-10
↓ mRNA MyD88
↓ phosphorylation NF-κB | ↓ 6 h mortality | [37] |
|
