INTRODUCTION: Fat grafting to the breast has a questionable oncologic risk according to laboratory reports on adipose tissue. One possible reason for this is the theoretical chronic inflammation due to adipokynes released by the grafted white adipose tissue (WAT).1–4 Thus, a translational study was designed to analyze inflammatory activity in lipofilled breast through proinflammatory markers. METHODS: Fifty-four paired-breasts of female rats were divided into three groups (control, grafted with autologous WAT of subcutaneous, and of omentum). The procedures of WAT preparation and grafting were performed as described previously.1–5 Briefly, a piece of WAT was harvested from omentum or subcutaneous and manually chopped with a scalpel into very small pieces and then placed into a 10-ml syringe. The WAT was then transferred into another 10-ml syringe through an emulsifier; in this way, the samples were homogeneously fragmented. Next, the samples were centrifuged at 3,000 rpm for 3 minutes. The lower and uppermost levels were discharged, such that only the middle layer (containing viable cells) was transferred into a 1-ml syringe. Finally, 0.2 ml of prepared autologous WAT (from omentum or subcutaneous tissue) was grafted through a 0.9-mm diameter cannula with a blunt tip into each of the 6 thoracic breasts of each rat. The rats were euthanized at 8 weeks post-operatively, and their breasts were harvested for analysis of gene quantification (via real-time PCR) for Mcp-1, F4/80, Cox-2 and IL-6. Statistical analyses were performed using paired t-tests, analysis of variance (ANOVA, one way) and Tukey’s test (post hoc). RESULTS: The markers Mcp-1, F4/80 and Cox-2 were similarly expressed among the groups (respectively p=0.422, p=0.143 and p=0.209). The expression of IL-6 marker was different between samples of breast grafted with WAT of omentum and subcutaneous (p=0.015), but not between samples of control and omentum (p=0.752), and control and subcutaneous (p=0.056). CONCLUSION: The difference in fold-change for IL-6 only between groups of lipofilled breasts, but not with control, certainly resulted from the different concentration of WAT of omentum and subcutaneous (they are from different embryological origin) in the breast composition in each group. Our results showed that no inflammation activity was identified in the lipofilled breast microenvironment, this illustrates that the tumorigenic potential of WAT reported for the mammary gland (regarding chronic inflammation) was not identified in our study. Reference Citations: 1. Claro, F., Jr., Moreira, L. R., Morari, J., et al. Assessment of the Cancer Risk of the Fat-Grafted Breast in a Murine Model. Aesthet Surg J 2016. 2. Gutowski, K. A., Force, A. F. G. T. Current applications and safety of autologous fat grafts: a report of the ASPS fat graft task force. Plast Reconstr Surg 2009;124:272–280. 3. Claro Jr, F., Figueiredo, J. C. A., Zampar, A. G., Pinto-Neto, A. M. Applicability and safety of autologous fat for reconstruction of the breast. British Journal of Surgery 2012;99:768–780. 4. Manabe, Y., Toda, S., Miyazaki, K., Sugihara, H. Mature adipocytes, but not preadipocytes, promote the growth of breast carcinoma cells in collagen gel matrix culture through cancer–stromal cell interactions. Journal of Pathology 2003;201:221–228. 5. Coleman, S. R. Structural fat grafting. St. Louis: Quality Medical Publishing; 2004.