From a Science Magazine online article:
They found that these physically active mice had fewer inflammatory cells (leukocytes) than sedentary mice, an effect they traced to diminished activity of hematopoietic stem and progenitor cells (HSPCs). The lower activity of HSPCs was due at least in part to exercise-induced reduction in the levels of leptin, a hormone produced by fat tissue that regulates cells within the hematopoietic bone marrow niche.
Regular physical activity is associated with a lower rate of death from heart disease, but the underlying mechanisms are not fully understood. Frodermann et al. examined the effect of exercise on cardiovascular inflammation, a known risk factor for atherosclerosis, by studying mice that voluntarily ran for long distances on exercise wheels.
To read more: https://science.sciencemag.org/content/366/6469/1091.2
Infections with the Enterococcus bacterium are a major threat in healthcare settings. They can lead to inflammation of the colon and serious illnesses such as bacteremia and sepsis, as well as other complications.
Their previous research has shown that when harmless strains of microbes are wiped out, often due to treatment with antibiotics, Enterococcus and other harmful types of bacteria can take over due to lack of competition. As part of the new study, which included analysis of microbiota samples from more than 1,300 adults having BMTs, the team confirmed the link between Enterococcus and GVHD.
“What you want is more, small fat cells rather than fewer, large fat cells,” Jackson said. “A large fat cell is not a healthy fat cell. The center is farther away from an oxygen supply, it sends out bad signals and it can burst and release toxic contents.” Large fat cells are associated with insulin resistance, diabetes and inflammation, he added.
“These results show quite clearly that there’s a very specific part of the brain network that’s affected by inflammation,” noted Mazaheri. “This could explain ‘brain fog’.”
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