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Antibiotics can make melanoma worse

“Any disease or therapy that damages the gut microbiome can have a negative impact on our health,” said Dr. Pal, who presented the report today at the annual meeting of the American Society of Bone and Mineral Research in Austin, Texas, US. ”

“In our study we found that the gut microbiome inhibits the progression of melanoma bone lesions in mice by promoting the expansion of intestinal natural-killer (NK) cells and T helper (Th1) cells, and their migration to the tumor site, ” Doctor. Paul said. “The use of oral antibiotics reduced the gut microbiome and reduced populations of intestinal NK cells and Th1 cells. This made the mice more susceptible to tumor development. They had more melanoma tumors than control mice. whose gut microbiome was intact.”

Osteolytic bone metastasis is a complication of malignant melanoma. The researchers hypothesized that using antibiotics to eliminate the mice’s gut microbiome would affect their intestinal immune cells and thus alter their immune response, leading to accelerated bone metastasis. They injected B16-F10 melanoma cells into the hearts and bones of mice that had been treated with broad-spectrum antibiotics. As predicted, the antibiotic injection accelerated bone metastatic growth in those mice, compared with control mice that did not receive the shot.

Metastatic evolution of melanoma: new insights

The study revealed the mechanism for the metastatic development of melanoma. Flow cytometric analysis of Peyer’s patches and bone-marrow cells within tumor lesions showed that microbiome depletion attenuated melanoma-induced expansion of intestinal NK and Th1 cells and their migration from the intestine to tumor-bearing bones. stopped. Direct measurement of the migration of NK and Th1 cells using Kaede mice, a strain expressing a photo-convertible fluorescent protein that allows direct tracking of intestinal lymphocytes, revealed that antibiotics increased NK and Th1 cells. There is an approximately eight-fold reduction in migration of K from the intestine to the tumor site. ,

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When NK cells and Th1 cells leave the gut as part of the body’s immune response, the process is mediated by the S1PR5 and S1PR1 receptors. Pharmacological blockade of migration of cells through receptors – involving S1PR5 with NK cells, or S1PR1 with Th1 cells – mimics the effect of antibiotics. The blockade prevented the expansion of NK cells and Th1 cells in the bone marrow and caused the accelerated development of bone metastasis. The flux of circulating NK and Th1 cells to the tumor site is directed by the chemokine ligand CXCL9, which is expressed by bone-marrow cells, and CXCR3, which is expressed by NK and Th1 cells. Global deletion of CXCR3 or antibody neutralization of CXCL9 decreased the frequency of tumor NK and Th1 cells and increased tumor growth.

“For example, inflammatory bowel disease, or other gut conditions that cause inflammation, can lead to increased Th17 cells, TNF producing cell numbers in the gut, which ultimately negatively impacts our bone health. Similarly, we have observed that in a murine model of surgical menopause, reduced levels of estrogen cause bacterial metabolites to pass through the gut barrier more readily and activate the immune system. As a result, intestinal T cells producing And bone marrow cytokine numbers are increased, which contributes to the development of massive bone loss.”

Dr. Pal continued: “We must be very mindful of the unexpected adverse consequences of our gut microbiome and antibiotic regimen. Conversely, probiotics may play a major role in maintaining a healthy gut microbiome and better overall health.”

Source: Eurekalert

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