Inflammatory bowel disease (IBD) is a chronic condition in which our body’s immune system mistakenly attacks the gut, causing symptoms such as abdominal pain, diarrhea, and weight loss due to inflammation. The biggest challenge in Crohn’s and colitis research is solving the mystery of its exact cause – or causes.
A potential factor being studied is the state of our gut microbiome - a diverse community of bacteria in the digestive tract, comparable to the diversity found in rainforests. These gut bacteria play a crucial role in daily health functions such as aiding in the digestion of stubborn fibers, and regulation of the immune system. In diseases like Crohn’s and colitis, there is often a reduction in our healthy gut bacteria diversity, synonymous with the loss of crucial insects in the rainforest: this process is known as dysbiosis (Fischbach et al., 2016). The loss of certain healthy bacteria in the gut leads to the overgrowth of harmful bacteria, potentially leading to Crohn’s or colitis. However, the specific bacteria involved are still unknown.
That is why it is especially impactful that recent advances in technology and research are leading to the identification of bacteria that can be used for diagnosis and treatment. Here is a summary of an encouraging research study published by Dr. Wine’s Team in the journal, Microbiome.
The study starts with our immune system, which is made up of immune cells called B cells and T cells. “Scouting” B cells travel through the body and produce immunoglobulins or molecular tags that bind to and identify foreign substances in the body. These molecules work by directing the second type of immune cells, “killer” T cells towards the foreign cell. Once the T cell finds its target, it engulfs the tagged foreign cells and removes it. Of the two types of immunoglobulins in our intestines––immunoglobulin A (IgA) and immunoglobulin G (IgG) –– IgG tags foreign substances, including harmful bacteria so that the “killer” T cells know which cells to eliminate. Patients with Crohn’s and colitis have higher IgG levels in their intestines.
To study the role of IgG, Wine and his team looked at the ability of different bacteria, some bound with immunoglobulin G (IgG) and some not, isolated from the guts of children with Crohn’s and colitis, to cause inflammation (Armstrong et al., 2019). They found that microbes tightly bound by IgG were more likely to inflame the guts of children with Crohn’s and colitis. Wine and colleagues suggest that when gut bacteria bind IgG, they function as indicators that can help medical professionals identify the bad strains causing Crohn’s and colitis. Researchers hope that IgG can be used as a marker for harmful bacteria in the guts of individuals with Crohn’s and colitis. IgG can also be used to develop diagnostics and treatments by targeting bacteria that trigger the body’s immune system to cause inflammation.
This innovative research in IgG-associated bacteria in Crohn’s and colitis not only sheds light on potential diagnostic tools but also exemplifies how academic research is contributing to enhancing the lives of individuals affected by these conditions, offering hope for more targeted and effective treatments in the future.
How does this discovery tie in with the GEM study?
The GEM study identifies novel causes and triggers of Crohn’s and colitis, which can range from certain genes to types of bacteria to certain lifestyle choices in individuals at risk for Crohn’s and colitis. This study by the Wine Team explores how IgG-associated bacteria help identify harmful bacteria and how it can be used as a potential diagnostic tool. This endeavor is a great example of academic research improving the quality of life of individuals with Crohn’s and colitis.
Fischbach, M. A., & Segre, J. A. (2016). Signaling in Host-Associated Microbial Communities. Cell, 164(6), 1288–1300. https://doi.org/10.1016/j.cell.2016.02.037
Armstrong, H., Alipour, M., Valcheva, R. et al. (2019). Host immunoglobulin G selectively identifies pathobionts in pediatric inflammatory bowel diseases. Microbiome 7, 1. https://doi.org/10.1186/s40168-018-0604-3