In 2019, it was estimated that 4.9 million people worldwide were living with inflammatory bowel disease (IBD), a condition for which there is currently no cure and whose exact cause is unknown. Researchers from Bar-Ilan University in Israel recently conducted a study involving a mouse model that suggests antibiotics could potentially harm the protective mucus layer of the gut, thus increasing the risk of developing IBD. Lead author Shai Bel and his team aimed to investigate the link between antibiotic use and IBD risk due to previous studies establishing a correlation between the two. Using advanced techniques such as RNA sequencing and machine learning, the researchers found that antibiotics such as ampicillin, metronidazole, neomycin, and vancomycin damaged the protective mucus layer in the digestive tract, allowing bacteria to penetrate and potentially increasing the risk of gut inflammation.
The study conducted by researchers at Bar-Ilan University revealed that the negative impact of antibiotics on the mucus barrier in the intestine was not caused by changes in the gut microbiome, but rather by direct alterations to the intestinal wall cells responsible for mucus production. This finding challenges the common assumption that antibiotics only affect bacteria and not human cells, shedding light on a previously unknown aspect of the effects of antibiotics on the body. The study also highlighted the potential risks associated with the overprescription of antibiotics, emphasizing the importance of using antibiotics judiciously and only when necessary. Further research is needed to explore additional factors that may be linked to antibiotic use in patients with IBD.
Harpreet Pall, MD, a pediatric gastroenterologist, commented that the study provided valuable insights into how antibiotics might increase the risk of developing IBD by disrupting the protective layer of the gut. He emphasized that understanding the risk factors for IBD could lead to the development of prevention strategies, earlier detection, and personalized treatment. Dr. Pall expressed hope that this research could lead to the identification of new potential treatment targets for IBD and pave the way for strategies to reduce the risk of developing the condition in high-risk patients.
Gastroenterologist Ashkan Farhadi, MD, also weighed in on the study, noting that it represents a significant shift in understanding the mechanisms by which antibiotics may influence the development of IBD. Farhadi highlighted the novelty of the study’s findings, as it is the first to demonstrate that antibiotics can impact human cells in the gut independently of changes to the microbiome. He acknowledged the need for further research to confirm these results and suggested that additional studies will be necessary to validate the data and potentially reshape current concepts about the effects of antibiotics on human cells.
The research conducted by the team at Bar-Ilan University offers new insights into the potential role of antibiotics in increasing the risk of developing IBD by damaging the protective mucus layer of the gut. By uncovering this direct effect of antibiotics on human cells in the gut, the study challenges conventional beliefs about the mechanisms by which antibiotics operate. Moving forward, continued research into the impact of antibiotics on the development of IBD will be essential to better understand the risk factors associated with the condition and potentially identify new avenues for prevention and treatment. These findings underscore the importance of using antibiotics judiciously and highlight the need for further investigations to validate and build upon the study’s results.
