Table 6:
Options: | Mechanism: | |
---|---|---|
Dysbiosis | Prebiotics, probiotics | Ingestion of live organisms or supplements to induce growth of certain commensal anaerobes |
Antibiotics | Depletion of pathogenic microbiota leading to overgrowth of healthy gut flora | |
Fecal microbial transplant | Transplantation of donor fecal samples | |
LPS | C11C1 | Monoclonal antibody that blocks LPS binding site |
CD14 antibodies | Lead to TLR4 internalization and decrease LPS response | |
Statins | Lead to increase expression of LDL-R and increase clearance of LPS | |
PCSK9 | Inhibit degradation of LDL-R leading to increase LPS clearance | |
IL-1B inhibitors | Block downstream TLR4 pathway leading to decrease in CVD | |
TMAO | FMO inhibitors | Block conversion of TMA into TMAO |
DMB | Inhibit microbial TMA lyases to inhibit production of TMA | |
CutC/D | Target microbial proteins |
C11C1, HMW Kininogen antibody; LPS, lipopolysaccharides; PCSK9, proprotein convertase subtilisin/ kexin type 9; LDL-R, low density lipoprotein receptor; IL, interleukin; TLR4,toll-like receptor 4; CVD, cardiovascular disease; FMO, Flavin monooxygenases; DMB, 3,3-dimethyl-1-butanol;