Human IL-6, IL-17, IL-1β, and TNF-α differently regulate the expression of pro-inflammatory related genes, tissue factor, and swine leukocyte antigen class I in porcine aortic endothelial cells.

摘要: Background Pro-inflammatory cytokines play important pathological effects in various diseases and allotransplantation; however, their role xenotransplantation remains elusive. In pig-to-human cell or organ transplantation, whether porcine cells organs are activated by human not as an question needs to be investigated. Methods We investigated the effect of IL-6, IFN-γ, IL-17, IL-1β, TNF-α using several vitro models aortic endothelial (PAECs) target cells. The downstream signaling pathways these were studied with Western blotting, regulation pro-inflammatory related genes pro-coagulation factor assessed real-time PCR enzyme-linked immunosorbent assay, swine leukocyte antigen (SLA) class I SLA II DR analyzed flow cytometry. Results We found that NF-κB mitogen-activated protein kinases (MAPKs) recombinant IL-17 (rhIL-17), rhIL-1β, rhTNF-α, while rhIL-6 signal transducer activator transcription 3 (STAT3) PAECs. adhesion molecules (E-selectin, VCAM-1, ICAM-1), gene (IL-6), chemokines (IL-8 MCP-1), (tissue factor) induced rhIL-17, only increased expression MCP-1 tissue factor. Using cytometry analysis, was upregulated PAECs after exposure rhIL-1β but whereas could rhIL-6, although it IFN-γ (rpIFN-γ). Although activation rhIL-17 alone strong, combined rhTNF-α amplified E-selectin, IL-8. Unexpectedly, we tocilizumab, a humanized anti-human IL-6 receptor antibody, block rhIL-6-mediated STAT3 Human activate STAT1 induce PAECs, which consistent previous report. Conclusion In conclusion, our data suggest significantly likely promote inflammation coagulation reaction response xenograft.