Medically reviewed by Onikepe Adegbola, MD, PhD
A study shows that enteric virome which are the components of gut microbiota shape inflammatory bowel disease phenotype. This mechanism happens through innate immune modulation. A recent study of Human enteric viruses autonomously shaping inflammatory bowel disease phenotype through divergent innate immunomodulation was published in the Journal of Science Immunology.
Immunomodulation of innate immunity is when cells are exposed to a priming substance or compound. Whereas, human viromes are diverse collections of all viruses found in humans or on humans. They include both prokaryotic and eukaryotic viruses
A Brief Comparison
Adiliaghdam and their team say they compared the composition and immunomodulatory function of the enteric virome of IBD (inflammatory bowel disease) patients. They tested those samples against the controls. Scientific controls are experiments or observations designed to minimize the effects of variables other than the independent variable. Comparing the control measurements to the other measurements increases the reliability of the results.
They treated human macrophages or intestinal epithelial cells with viral-like particles enriched from the site of inflammation. These particles were then administered to recipient mice for review.
The mice show the development of non-specific or innate immunity. As a result of infection and/or inflammation, macrophages acquire a high glycolytic activity phenotype.
As a result, IBD-associated enteric viromes exacerbate inflammation, while non-IBD-associated enteric viromes are protective and suppress their inflammatory properties.
Intestinal Homeostasis
The homeostasis of the intestinal microbiome relies on the physical separation of the majority of intestinal microbes from the mammalian immune system. Numerous biophysical and biochemical barriers take part in the process. To maintain the homeostasis of the organism, all organ systems in the bodywork together. Failure to maintain homeostasis can result in death or disease. After birth, the immune system can co-evolve with the microbiota, allowing the host and microbiota to coexist in a mutually beneficial relationship.
Hence, it is detrimental to intestinal and systemic health for a host to fail to achieve or maintain an equilibrium between its microbiota and itself.
In this study, scientists demonstrate that perturbations in enteric virome are detected by innate immune system sensors and subsequently affect intestinal homeostasis.
Eukaryotic viruses and bacteriophages from non-IBD, non-inflamed human colon resections were found to activate atypical anti-inflammatory immune responses. Viromes from a non-IBD patient successfully dampened inflammation induced by Crohn’s disease colon resection viromes.
While mice expressing IBD intestinal tissue viromes show enhanced intestinal inflammation as a result of nucleic acid-sensing.
IBD and the Effect of Virome
IBDs are the conditions resulting from a complex interplay between host, microbial, and environmental factors. Considering the dominance of bacteriophages, the interaction between microbiota and virome is not surprising.
The results provide some of the first functional evidence that the collective viruses in a normal/non-inflamed intestine can help humans build gut immunity in contrast to the common belief that viruses are harmful. Therefore, an alteration in the intestine-resident prokaryotic or eukaryotic virome has detrimental consequences for the human intestine and can directly contribute to IBD.
A new way to treat intestinal and immunological diseases could be therapeutic modulation of the virome. Researchers can achieve it through targeted elimination or replacement of disease- and health-causing intestinal viruses.
Reference:
Adiliaghdam, F., Amatullah, H., Digumarthi, S., Saunders, T. L., Rahman, R. U., Wong, L. P., Sadreyev, R., Droit, L., Paquette, J., Goyette, P., Rioux, J. D., Hodin, R., Mihindukulasuriya, K. A., Handley, S. A., & Jeffrey, K. L. (2022). Human enteric viruses autonomously shape inflammatory bowel disease phenotype through divergent innate immunomodulation. Science Immunology, 7(70), eabn6660. https://doi.org/10.1126/sciimmunol.abn6660
