Dear Editor It is with great interest to read the article by Wang et al. titled “The effects of macrophage‐mediated inflammatory response to the donor site on long‐term retention of… Click to show full abstract
Dear Editor It is with great interest to read the article by Wang et al. titled “The effects of macrophage‐mediated inflammatory response to the donor site on long‐term retention of a fat graft in the recipient site in a mice model” (Wang et al., 2020). The authors hypothesized that there is a competition of repair process mediated by inflammatory response between donor and recipient sites. The results showed that donor site was the prior one and reduced the retention of fat graft at recipient site. The idea was very novel with encouraging results, and we have some considerations and conjectures about the mechanism of the results. First, we believe it was inappropriate to conclude that macrophages at recipient site were insufficient at early stage due to the poor blood supply. Because the blood supply at recipient site in Grafting‐Only group and long‐time delayed groups was also poor, but the macrophages were not insufficient at early stage as shown in the results. We believe it is better to make blood supply be the only independent variable before concluding that blood supply is a factor affecting macrophages infiltration. To explain the possible mechanism of the priority of donor site in the possible existing competition, we speculate that it was the greater trauma rather than the good blood supply that recruited more macrophages, due to a stronger need of repair. The recipient site underwent only subcutaneous fat injection, while the donor site underwent skin incision, closure, and simulated liposuction by fat pads destruction. So as shown in the study, more inflammatory cytokines like interleukin (IL)‐1, IL‐6 and tumor necrosis factor‐α were stimulated at donor site, and more chemokines like CCL2 were released and subsequently attracted more macrophages to repair the trauma (Strieter et al., 1994). This conjecture which need further study also corresponded with the first suggestion put forward by the author, that the injury at the donor site should be minimized. To be added, the fat graft injection at recipient site in clinical practice is multilayer and multitunnel, which is much more invasive than one‐site injection used in this study. So the simulated surgery was supposed to be modified in this trauma inflammation related study. Second, it was interesting to found that the long‐term volume retention rate became normal in long‐time delayed groups. We conjecture that there may be a mechanism like remote ischaemic preconditioning, a chemical, mechanical, or electrical peripheral stimulus to harness the endogenous protective capabilities against injury (Hausenloy & Yellon, 2008; Heusch et al., 2015). The release of angiogenic cytokines like vascular endothelial growth factor and the recruitment signals for stem cells and macrophages from bone marrow were upregulated once the donor site was severely damaged. The reserve capability might be enhanced, consequently improving the vascularization and other protective function in all parts of the body including the recipient site. The myocardial infarct size could be dramatically reduced by preconditioning (Hausenloy & Yellon, 2008). As such, the fat could be supported in a better grafting bed and gain a higher retention rate. To be noticed, the effect of preconditioning may only be seen after 7 days or later, so there was no significant result in short‐time delayed group. According to that, we believe the grafting bed on the back should be tested just before injection in all delayed groups, to find whether the effect of preconditioning exists.
               
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