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The efficient operation of the immune system depends on the presence of B lymphocytes. However, Karolinska Institutet researchers have demonstrated that they can occasionally cause more harm than good since their numbers sharply increase following intestinal trauma, impeding the healing process.
The findings, which are published in the journal Immunity, may have an impact on how inflammatory bowel disease is managed. White blood cells known as B cells play a significant role in the immune system, in part by creating antibodies that fight viruses and bacteria. Previous studies have demonstrated that the number of B lymphocytes in the intestines is significantly higher in people with chronic inflammatory bowel disease (IBD), such as Crohn's disease or ulcerative colitis. It has therefore been proposed that B cells might affect the severity of these diseases. Researchers at Karolinska Institutet in Sweden have now tried to discover if, and if so how, B cells contribute to IBD. The sharp increase during healing: "We've been able to show that the B cell population increases sharply in the colon during the healing of colonic lesions and that these cells mainly accumulate in areas where the damage is severe," says principal investigator Eduardo Villablanca, associate professor at the Department of Medicine (Solna), Karolinska Institutet. "This prevents, in turn, the interaction between two other cell types - stromal and epithelial cells - which is needed for the tissue to heal." Using a variety of techniques for cell population analysis, the researchers looked at tissue from patients with ulcerative colitis and an experimental model of colitis. They discovered that animals lacking B cells recovered far more quickly after bowel injuries than typical mice, with specific attention paid to how B cells promote recovery in the intestinal mucosa. The discovery that B lymphocytes appear to cause more harm than good in colonic inflammation may have important implications for the management of IBD. Drugs that affect B cells: "There are already approved drugs that affect the B cell response and that are used for other diseases," says Gustavo Monasterio, a postdoc in Dr Villablanca's research group at Karolinska Institutet and one of the leading authors. "We now want to test if depleting B cells at specific time windows could also work with IBD. We also need to find out if the accumulation of B cells can have a long-term beneficial effect, such as by changing the composition of bacteria in the gastrointestinal tract." (ANI)
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