Table 2.
Nanotechnology for sepsis treatment
| Agents | Size (nm) | Target | Technique | Refs. | |
|---|---|---|---|---|---|
| Metal-based | AuNPs | 21 | M2 macrophages | AuNPs own antibiotics effect (only in vitro test) | [52] |
| Fe3O4-Ce6-Apt | 17 | Bacterial colony (live/death) | Magnetic enrichment for capturing blood disinfection | [42] | |
| SPION | 6.5 | Liver-resident macrophages | Increasing IL-10 and attenuate organ damage by autophagy | [53] | |
| mSPAM | 97 | Intracellular levels of H2O2 | Suppression of HIF-1α-mediated NF-κB activation | [54] | |
| Polymer-based | Atv/PTP-TCeria NPs | 8 | ROS level in kidney | ROS downregulation drug delivery (atorvastatin) | [48] |
| CIP-NPs-Abs | 120 | Infectious microenvironments (I-CAM1) | Co-delivery of antibiotics and anti-inflammatory cytokine | [55] | |
| DNase-I pMNSs | 170 | NETosis by Neutrophils | Delivery of DNase-I | [56] | |
| Lipid-based | VCLNPs | 127–174 | AMP-Cathepsin B macrophage | Delivery of AMP with CatB mRNA | [47] |
| M-Lipo | 200 | LPS in the blood fluid | Absorption of LPS and endotoxin | [57] | |
| Leukosome | 94 | Macrophages | Cytokine control: reduce the pro-inflammatory genes (IL-6, IL-1b, and TNF-α) regulation and increase anti-inflammatory ones (IL-10 and TGF-β) | [58] | |
| Others | TMD | – | ROS and RNS | Scavenging activity and sustainability for H2O2, O2·–, OH· | [59] |
| TD-NT | – | Pro-inflammatory cytokine, DAMP and PAMP | Charge-dependent (negative) size exclusive (~ 50 kDa) | [60] |