Breast cancer is one of the most common cancers in women， which seriously threatens women's health. Early diagnosis and precise treatment of breast cancer are helpful to improve the prognosis of patients. This article summarizes the research status of bacteria and their metabolites in the development and treatment of breast cancer， and discusses in detail the role and mechanism of bacteria and their metabolites in the development and intervention of breast cancer. These mechanisms include regulation of inflammation and immune response， DNA damage， and regulation of cell biological characteristics. Engineering bacteria have become one of the hotspots in the field of breast cancer treatment in recent years due to their natural advantages in targeting tumors and activating immunity. This article further summarizes the research progress of engineered bacteria in the treatment of breast cancer， aiming to provide an important reference for formulating targeted treatment strategies and improving the prognosis of patients. Although bacteria and their metabolites affect the development and treatment of breast cancer through a variety of mechanisms， and can enhance the therapeutic effect of cancer and reduce the adverse effects of treatment， the clinical application of bacteria in anti-breast cancer therapy still faces numerous challenges. The highly individualized composition of bacteria leads to the lack of universality of treatment， and the complex interaction between bacteria and host further increases the difficulty of research. In the future， it is urgent to further explore the mechanism of bacteria and their metabolites affecting the development and treatment of breast cancer， and promote the clinical application of bacteria in anti-breast cancer treatment.

[Objective]Depression is a common mental illness with a profound impact on physical health.Depression has been associated with a higher risk of bacterial infection;however,whether this relationship is causal and how depression affects infection remains unclear.Therefore,we aimed to investigate the effects of depressive phenotype in infected mice by constructing a chronic unpredictable mild stress(CUMS)model.[Methods]Mice were induced with CUMS for 4 weeks.The depressive phenotype was evaluated using behavioral tests.Subsequently,the mice were intraperitoneally injected with Klebsiella pneumoniae to establish bacterial infection.Serum and abdominal tissues were collected 48 h after infection.Hematoxylin-eosin(HE)staining was used to observe the pathological changes in the tissues,and enzyme-linked immunosorbent assay(ELISA)was used to measure the levels of inflammatory factors.In addition,the fecal samples collected before infection were analyzed for 16S rDNA gene of gut microbiota,and the expression levels of NF-κB/NLRP3 signaling pathway in colon tissues of uninfected mice were detected.[Results]Behavioral tests showed that compared with the control mice,CUMS mice had significantly lower body weight(P<0.0001,t=5.426),lower sucrose preference rate(P<0.001,t=4.937),increased swimming stationary time(P<0.001,t=16.37),and decreased time spent in the central area of the open field(P<0.01,t=3.575).Survival analysis showed that compared with the control mice,the survival rate of CUMS mice significantly decreased after infection(P<0.05).Additionally,histochemical staining showed that tissue damage in the liver(P<0.05,t=4.025),kidney(P<0.05,t=2.828),and mesentery(P<0.01,t=5.367)significantly increased.Furthermore,ELISA results showed that the levels of the inflammatory cytokines IL-6(P<0.01,t=3.365),IL-1β(P<0.01,t=4.061),TNF-α(P<0.01,t=4.460)and LPS(P<0.0001,t=27.24)were elevated.The difference was statistically significant.According to 16S rDNA sequencing,CUMS-induced changes in the intestinal bacterial community structure of mice,making them significantly different from the control mice.Compared with the control mice,the expression levels of NF-κB(P<0.01,t=6.825)and NLRP3(P<0.001,t=9.561)were upregulated in CUMS mice.[Conclusion]The CUMS model was successfully constructed and CUMS mice developed more severe bacterial infection.Gut microbiota was dysregulated and the expression of NF-κB/NLRP3 signaling pathway was up-regulated in CUMS mice,which was related to the susceptibility to bacterial infection.