 Hi, my name is Carolina Serena, and they are Noelia Kailan, Joan Vendrell, and Sonia Fernández. We are a research group from Tarragona Spain, and we would like to show you a video summarizing the study we just published in stem cells. However, before to see the video, we would like to introduce a topic for a little perspective. In the last years, a deposition has been proposed as an interesting alternative source of mesenchymal stem cells for regenerative cell therapy. In fact, it has been demonstrated that the immunomodulatory properties of adipose stem cells are more potent than those right from bone marrow. That is why, apart from being the main energy storage depot, adipostitium should be considered as an immune organ at the crossroads between metabolism and immunity. In this context, local factors of adipostitium may be taken into consideration and we hypothesize that the donor phenotype determines the immunotonic capacity of adipose-derived stem cells. So, our work highlights the importance of studying stem cells, taking into consideration their physiological environment. Moreover, it is also relevant not only for understanding the functionality of adipose-derived stem cells in terms of cell-based therapies, but also for the role as key regulators of kidney response. So, enjoy the video and thank you. Obesity is an associated state of chronic low-grade inflammation. Adipostitium is now considered as a bona fide immune organ at crossroads between metabolism and immunity. Besides adipocytes, adipostitium contains macrophages, lymphocytes and adipose-derived stem cells. ACs first participate in the turnover of mature adipocytes. Second, have certain igual capacity. And finally, are recruited to sites of tissue damage to regenerating tissues and repair the effects. But if the function of these cells is affected by obesity, it is still unknown. Focusing on obesity and diabetes as metabolic disorders that might affect the immune response of ACs, we obtain tissue biopsies from different donors. Adipose tissue is digested with collagenase in order to obtain the stromal vascular fraction from which ACs are isolated. It is really important to phenotype the human AC population. We use flow cytometry. Obes and particularly diabetic ACs show an increase of inflammatory markers with a high secretion of interlocking guanbeta. Given that inflammasome signaling mediates interlocking guanbeta secretion, we check the protein expression of the main inflammasome components. Interestingly, a significant activation of these components were observed in ACs from obese and diabetic individuals. Our data reveals that ACs from obese and diabetic patients are able to migrate and invade other tissues. ACs from lean subjects were unable to invade. By contrast, ACs from obese and diabetic patients showed a robust invasion capacity. Accordingly, the metalloprotease activity was higher in obese and diabetic ACs. Since immigration and invasion are crucial steps for phagocytosis, we hypothesize that ACs might be acting as nonprofessional phagocytes. Interestingly, ACs from lean or obese and diabetic subjects could phagocyte bacteria. Furthermore, obese and diabetic ACs show a higher phagocytic activity than lean ACs. Emerging evidence suggests that ACs might affect the properties of immunomodulatory cells. First, we observe increased engine expression and secretion of the transforming growth factor beta-1 in obese and diabetic ACs. Second, it is known that conditioning media from lean ACs promotes M2 macrophage phenotype anti-inflammatory. We observe that conditioning media from obese and diabetic ACs promotes M1 macrophage phenotype inflammatory. And third, conditioning media from lean ACs suppress TMB cell proliferation. By contrast, conditioning media from obese and diabetic increase significantly TMB cell proliferation. To corroborate these results, TMB cell proliferation was visualized using Verde-U immunofluorescence. Given that inflamosome-induced interlocking 1-beta secretion was activated in obese and particularly diabetic ACs, we pre-treat healthy ACs with interlocking 1-beta and significantly increase cell migration and confer invasion capacity. Conversely, treatment of obese and diabetic ACs with Tg-beta-1 combined with interlocking 1-beta receptor antagonists significantly decreases cell migration. Nonetheless, our study unveils both Tg-beta-1 and interlocking 1-beta as potential key players in the dysfunctional AC behavior observed in these metabolic pathologies. To sum up, obese and diabetic ACs have a higher migratio-invasion-anctagocytic capacity, unless immunosuppressive properties than lean ACs.