FIGURE 3
Potential involvement for macrophages that have been triggered by the microbiome in the tumor microenvironment. (A) By modifying the expression of intermediate metabolites, activated macrophages can modify glucose metabolism, iron cycling, and lipid metabolism and control the tumor microenvironment. (B) Activated macrophages release a variety of cytokines, chemokines, and growth factors that influence tumor formation by boosting cell proliferation and decreasing the activity of immune cells that can destroy tumors, like cytotoxic T cells. (C) Macrophage-derived exosomal miRNAs alter the immunological milieu by targeting proteins and activating molecules.
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Cancer and microbial infections are significant worldwide health challenges. Numerous studies have demonstrated that bacteria may contribute to the emergence of cancer. In this review, we assemble bacterial species discovered in various cancers to describe their variety and specificity. The relationship between bacteria and macrophages in cancer is...
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Macrophages are crucial components of the immune system and play a critical role in the initial defense against pathogens. They are highly heterogeneous and plastic and can be polarized into classically activated macrophages (M1) or selectively activated macrophages (M2) in response to local microenvironments. Macrophage polarization involves the r...
Citations
... As the largest and most complex ecosystem in the human body, the intestinal flora and its thousands of metabolites influence almost every aspect of the host's physiological activity (69). Although most microbes are engulfed and killed by macrophages, some bacteria live inside macrophages as opportunistic residents and use them to replicate (70). M1 macrophages can be controlled by microbial stimuli, including intracellular bacteria, to support cytotoxic activity and infection resistance. ...
... To avoid cytotoxic effects and evade the cellular immune response, microbes such as Fusobacterium nucleatum possibly promote M2polarised macrophages (71). When host pathogens interact, live bacteria or their components often trigger innate immune cell reactions and cause immune cells, such as macrophages, to migrate towards tumours (70). Data show that microbial pathogens play a carcinogenic role in gastrointestinal tumorigenesis (72). ...
... Studies have shown that inflammation caused by H. pylori infection is associated with expression of TLR4 and TLR9. Furthermore, TLR9 plays a major role in the inflammation occurring in GC (70). Once PAMPs are recognised, TLRs induce polarisation of TMAs by activating activator protein (AP)-1, interferon regulatory factor (IRF) and NF-kB, which promote expression of inflammatory mediators such as TNF-a, IL-1, IL-2, IL-6, IL-8, IL-12 and INF-g (79). ...
As one of the deadliest cancers of the gastrointestinal tract, there has been limited improvement in long-term survival rates for gastric cancer (GC) in recent decades. The poor prognosis is attributed to difficulties in early detection, minimal opportunity for radical resection and resistance to chemotherapy and radiation. Macrophages are among the most abundant infiltrating immune cells in the GC stroma. These cells engage in crosstalk with cancer cells, adipocytes and other stromal cells to regulate metabolic, inflammatory and immune status, generating an immunosuppressive tumour microenvironment (TME) and ultimately promoting tumour initiation and progression. In this review, we summarise recent advances in our understanding of the origin of macrophages and their types and polarisation in cancer and provide an overview of the role of macrophages in GC carcinogenesis and development and their interaction with the GC immune microenvironment and flora. In addition, we explore the role of macrophages in preclinical and clinical trials on drug resistance and in treatment of GC to assess their potential therapeutic value in this disease.
Gynecological and obstetric infectious diseases are crucial to women’s health. There is growing evidence that links the presence of Fusobacterium nucleatum (F. nucleatum), an anaerobic oral commensal and potential periodontal pathogen, to the development and progression of various human diseases, including cancers. While the role of this opportunistic oral pathogen has been extensively studied in colorectal cancer in recent years, research on its epidemiological evidence and mechanistic link to gynecological diseases (GDs) is still ongoing. Thus, the present review, which is the first of its kind, aims to undertake a comprehensive and critical reappraisal of F. nucleatum, including the genetics and mechanistic role in promoting adverse pregnancy outcomes (APOs) and various GDs, including cancers. Additionally, this review discusses new conceptual advances that link the immunomodulatory role of F. nucleatum to the development and progression of breast, ovarian, endometrial, and cervical carcinomas through the activation of various direct and indirect signaling pathways. However, further studies are needed to explore and elucidate the highly dynamic process of host–F. nucleatum interactions and discover new pathways, which will pave the way for the development of better preventive and therapeutic strategies against this pathobiont.
