In the recent years, it has been evidenced an important connection between the immune system and intestinal microorganisms in the development of obesity, metabolic syndromes and cardiovascular diseases. We have shown that a single episode of intestinal infection by Yersinia pseudotuberculosis (YP) is capable of inducing a phenomenon known as "immunological scarring", which includes chronic inflammation of the mesenteric adipose tissue (MAT) and mesenteric lymph node (mesentery), a permanent damage of mesenteric lymph vessels, associated with changes in lipid traffic and a limited capacity for using lipids as an energy source despite the presence of improved glucose disposal due to an improvement on insulin sensitivity. We named this process as a non-classical metabolic syndrome. In this study, we investigated the mechanisms sustaining the immunological scar, as well as the metabolic changes induced by YP infection. Initially, we tested whether changes in the gut microbiota could be associated with the metabolic alterations by YP. We verified that this association exists, but that it does not seem to be related to a higher production of short-chain fatty acids by the intestinal microbiota after YP infection. Thus, we evaluated the impact of the MAT and mesenteric lymph node remodeling resulting from YP infection on the development of the non-classical metabolic syndrome. Therefore, we searched for different strategies to reverse the mesenteric inflammation and its the interference in the insulin response. For this purpose, we tested the treatment with glibenclamide (which blocks NLRP3), in order to reduce the inflammation in the mesentery, and two strategies to restore the homeostatic type 2 immunity in the MAT by the immunization with ovalbumin (OVA) plus alum adjuvant. However, none of these strategies was able to reverse inflammation in the mesentery, as well as to satisfactorily return the canonical immune response in the MAT, even though it proved to be satisfactory for the return of an insulin response closer to homeostatic levels. Furthermore, we evaluated the contribution of the B lymphocytes in the MAT induced by YP infection on the insulin response, by using mice deficient for mature B cells (B-KO). We found that the absence of mature B cells completely abrogated the increased insulin sensitivity induced by YP infection. Finally, we evaluated the functional impact of the changes in lipid traffic induced by YP infection, using an experimental model of atherosclerosis by feeding of ApoE deficient mice with a hypercholesterolemic diet (HCD). We observed that the previous infection with YP increased the susceptibility to the development of atherosclerosis. Thus, our data suggest that other long-term effects of YP infection may include the impairment of induction of type 2 immunity, locally and systemically, and increased susceptibility to the development of cardiovascular diseases, including atherosclerosis. Also, B cells seems to play a role in the metabolic changes induced by YP infection.