It is not clear whether gut inflammation has a causal role in myeloproliferative neoplasms, or the other way around.
The microbiomes of patients with myeloproliferative neoplasms (MPN) have significant differences from the microbiomes of healthy controls, according to a new study, and the variations appear to promote inflammation.
The report, published in the journal Microbiology Spectrum, adds new layers to scientists’ understanding of MPN, but also underscores the important role of the gut microbiome in various diseases.
Corresponding author Angela G. Fleischman, M.D., Ph.D., of the University of California, Irvine, and colleagues, noted that the gut microbiome has lately been the topic of significant research related to acute myeloid leukemia and hematopoietic stem-cell transplantation. However, they said no studies have looked at how the gut microbiome might affect MPN.
Given the central role of inflammation in MPN, Flesichman and colleagues said there was good reason to question whether there might be an association between MPN and the gut microbiome.
“The inflammation in MPN is multifactorial, and the neoplastic clone itself induces inflammation,” they wrote. “However, chronic inflammation may precede the development of MPN and play a critical role in disease initiation.”
They noted that MPN can manifest differently from patient to patient, a fact that could be the result of forces beyond MPN itself affecting inflammation levels.
The investigators decided to analyze the composition of the gut microbiomes of patients with MPN, and compare those findings to samples taken from healthy controls. They recruited 25 patients with MPN and 25 controls, collecting 3 fecal samples from each participant over the course of one week. They then conducted gene sequencing and analysis to better understand the composition of the subjects’ microbiomes.
Broadly speaking, there was very little disease-related difference between the MPN and non-MPN samples. The authors said most of the variance between samples was based on individual factors. Yet, 1.7% of the variance between cohorts appeared to be related to disease status, the authors found.
More specifically, the MPN samples had lower levels of species of Phascolarctobacterium, which has been associated with inflammation reduction. The investigators also identified a possible association between the genus Parabacteroides and the inflammatory cytokine tumor necrosis factor-α, which was elevated in the MPN samples.
Fleischman and colleagues said that finding seems to align with earlier research.
“Interestingly, one study found a species of Parabacteroides to be enriched in patients with colorectal carcinoma,” they wrote.
However, they also noted that levels of Parabacteroides appeared to be affected by diet. Patients with greater intake of fruits and vegetables tended to have lower abundance of Parabacteroides.
“Conceivably, dietary nutrients such as vitamins and fiber may be an important covariate in the management of inflammatory diseases such as MPN,” they said. “For example, low-fiber diets are associated with colonic inflammation and can be lessened by switching to a high-fiber diet, coincident with changes in colonia microbial metabolism.”
The implications of diet on MPN require further study, the investigators said, as do questions of whether products like probiotics or therapies like fecal transfer might affect MPN by changing a patient’s microbiome. They added that it might also be possible that MPN therapies are already affecting the microbiomes of patients with MPN.
As investigators ponder those questions, one larger question remains: does the microbiome have a causal role in MPN, or does MPN exaggerate the inflammatory response in the microbiome?
For now, Fleischman and colleagues said, that question remains unanswered. However, they said this study acts as an important first step toward finding an answer.
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