Regulatory B cells are specific white blood cells that are involved in protecting the body and have the ability to differentiate (or turn into) other types of immune cells in response to inflammation in the body. Their role is to regulate and restrain immune responses by producing the anti-inflammatory interleukin-10 but it is unclear what specific signals cause regulatory B cells to differentiate. In an article published in Nature Medicine, a team of scientists explored the effects of changes to the gut microbiome in mice on the differentiation abilities of regulatory B cells.
The authors studied a control group of conventionally housed mice with groups of mice treated with various antibiotics, including vancomycin, neomycin, and metronidazole. Mice treated with antibiotics had the majority of their gut microbiome eliminated and as a result developed milder arthritis, showing that the microbiome is responsible for the induction of arthritis. It was also found that the mice that were treated with antibiotics had reduced numbers of undifferentiated precursor B cells.
The authors later recolonized the gut microbiome of antibiotic-treated mice using fecal samples of the control mice. Examination of the regulatory B cells of the newly recolonized mice showed suppressive activity of arthritis inflammation. To examine if changes in housing had an effect on regulatory B cells, the researchers also studied conventionally raised mice compared to mice housed in a specific pathogen-free environment and this group showed reduced regulatory B cell activity.
In this study, the authors showed a strong correlation between the gut microbiome of mice and immune system inflammatory response to pathogens. This study also suggests that an overuse of antibiotics will not only deplete our gut microbiome as we have seen in several previous studies, but also reduce the function and differentiation of our regulatory B cells that play a critical role in our immune system function.