Advancements in the impact of human microbiota and probiotics on leukemia

Abstract

The human gut microbiota is a complex ecosystem that plays a crucial role in promoting the interaction between the body and its environment. It has been increasingly recognized that the gut microbiota has diverse physiological functions. Recent studies have shown a close association between the gut microbiota and the development of certain tumors, including leukemia. Leukemia is a malignant clonal disease characterized by the uncontrolled growth of one or more types of blood cells, which is the most common cancer in children. The imbalance of gut microbiota is linked to the pathological mechanisms of leukemia. Probiotics, which are beneficial microorganisms that help maintain the balance of the host microbiome, play a role in regulating gut microbiota. Probiotics have the potential to assist in the treatment of leukemia and improve the clinical prognosis of leukemia patients. This study reviews the relationship between gut microbiota, probiotics, and the progression of leukemia based on current research. In addition, utilizing zebrafish leukemia models in future studies might reveal the specific mechanisms of their interactions, thereby providing new insights into the clinical treatment of leukemia. In conclusion, further investigation is still needed to fully understand the accurate role of microbes in leukemia.

Keywords: gut microbiota; leukemia; leukemia treatment; probiotics; zebrafish models.

Figure 1

The pathogenesis and leukemia classification. (A) The development of leukemia involves various genetic abnormalities, including chromosome crossovers, deletions, and point mutations. (B) Abnormal proliferation of hematopoietic stem cells can lead to leukemia. Leukemia is divided into chronic leukemia and acute leukemia. Chronic leukemia is characterized by slow onset of peripheral blood or bone marrow cells, which can be divided into CML and CLL. A decrease in mature leukocytes and an impaired immune response may result in acute leukemia. Acute leukemia can be divided into AML and ALL.

Figure 2

The involvement of probiotics in different stages of tumor development helps in personalized treatment and prognosis of the disease. (A) Single strains or combinations of strains can be used as diagnostic and early-stage biomarkers to help determine the occurrence or development of tumors, and personalized microbiome therapy can be applied. (B) During the treatment period of leukemia, the beneficial bacteria selected from the bacterial strain library can not only regulate the proliferation and apoptosis of tumor cells at the cellular level, but can also be used in conjunction with chemotherapy drugs to improve the effect of chemotherapy and reduce the adverse reactions caused by chemotherapy. Engineered probiotics can improve the efficacy of immunotherapy in mouse tumor models through metabolic regulation of the tumor microenvironment. Fecal microbiota transfer (FMT) has been developed to restore diverse microbial communities lost during subsequent treatment in patients with acute myeloid leukemia, thereby suppressing, reducing or even preventing treatment-related complications. (C) Therapeutic benefits to the prognosis of cancer patients by modulating dietary and balanced nutritional intake and enhancing the gut microbiota through dietary fiber-gut microbiota related mechanisms affecting the patient’s cancer treatment response to immunotherapy.

Figure 3

The anti-inflammatory and anti-proliferative effects of anti-cancer drugs or probiotics. The anti-inflammatory and decreasing cancer cell proliferation effects of anti-cancer drugs or probiotics on cancer cell. (A) The anti-cancer effect of mercaptopurine potentially functions by reducing IL-6 and TNF-α levels and increasing short-chain fatty acids (SCFAs) mediated by the gut microbiota. (B) Bacillus subtilis induces both the anti-inflammatory factor IL-10 and the pro-inflammatory factor IL-12 in THP-1 dendritic cells. (C) Bifidobacterium bifidum reduces cancer cell proliferation by inhibiting growth factor signaling and promoting mitochondria-mediated apoptosis proliferation.