The Microbiome and Autoimmunity

pablo

 

Scientists have long suspected a link between inflammatory bowel disease, psoriasis, and arthritis, since the same patients are often afflicted with more than one of these conditions.  As new technologies have enabled detection of invisible gut inflammation, it has become clear that in people with arthritis or psoriasis, gut inflammation is not the exception, but the rule.

The precise causes of this gut inflammation are not fully understood, but the latest evidence points to a significant role of the microbiome—the vast community of bacteria that resides in our gut.  One of the early discoveries in this area was made by a French gastroenterologist named Dr.Harry Sokol, who found that patients with Crohn’s disease (a form of inflammatory bowel disease) had lower levels of one particular bacterial species, F. prausnitzii.[i]  In the years since, the critical role of this species has emerged: it is a peacekeeper that helps to regulate the immune system, by boosting anti-inflammatory immune cells. It also helps to preserve the integrity of the gut barrier, thereby segregating harmful bacteria and toxins from the circulation and immune system.

In the years since Dr. Sokol’s discovery, there has been a massive global effort to understand the impact of the microbiome on inflammatory disease.  Further pieces of the puzzle have begun to fall into place, with the discovery that other related bacterial species fulfill the same peacekeeping function as F. prausnitzii, preserving the gut barrier and calming the immune system.

In 2015 and 2016, several groups of researchers made the groundbreaking discovery that particular species of gut bacteria that regulate the immune system are often depleted in those with psoriasis, psoriatic arthritis, juvenile arthritis, and ankylosing spondylitis.[ii]  These conditions, along with rheumatoid arthritis, are also associated with an increased prevalence of undesirable gut bacteria, such as E.coli.[iii]  In short, the balance of the microbiome is disrupted in those with psoriasis or arthritis, with a reduction in anti-inflammatory species and an increase in species that can spark an immune response.

Fortunately, the latest research also provides a road map for restoring the balance of the microbiome, through diet and carefully chosen probiotics, as my new book explains.

 

 

References

 

 

[i] Sokol, H., Pigneur, B., Watterlot, L., Lakhdari, O., Bermúdez-Humarán, L. G., Gratadoux, J. J., … & Grangette, C. (2008). Faecalibacterium prausnitzii is an anti-inflammatory commensal bacterium identified by gut microbiota analysis of Crohn disease patients. Proceedings of the National Academy of Sciences, 105(43), 16731-16736.

[ii] Scher, J. U., Ubeda, C., Artacho, A., Attur, M., Isaac, S., Reddy, S. M., … & Manasson, J. (2015). Decreased bacterial diversity characterizes the altered gut microbiota in patients with psoriatic arthritis, resembling dysbiosis in inflammatory bowel disease. Arthritis & rheumatology, 67(1), 128-139.

Di Paola, M., Cavalieri, D., Albanese, D., Sordo, M., Pindo, M., Donati, C., … & Lionetti, P. (2016). Alteration of Fecal Microbiota Profiles in Juvenile Idiopathic Arthritis. Associations with HLA-B27 Allele and Disease Status. Frontiers in Microbiology, 7.

Eppinga, H., Weiland, C. J. S., Thio, H. B., van der Woude, C. J., Nijsten, T. E., Peppelenbosch, M. P., & Konstantinov, S. R. (2016). Similar depletion of protective Faecalibacterium prausnitzii in psoriasis and inflammatory bowel disease, but not in Hidradenitis suppurativa. Journal of Crohn’s and Colitis, 10(9), 1067-1075.

Stoll, M. L., Kumar, R., Morrow, C. D., Lefkowitz, E. J., Cui, X., Genin, A., … & Elson, C. O. (2014). Altered microbiota associated with abnormal humoral immune responses to commensal organisms in enthesitis-related arthritis. Arthritis research & therapy, 16(6), 486.

[iii] Viladomiu, M., Kivolowitz, C., Abdulhamid, A., Dogan, B., Victorio, D., Castellanos, J. G., … & Chai, C. (2017). IgA-coated E. coli enriched in Crohn’s disease spondyloarthritis promote TH17-dependent inflammation. Science Translational Medicine, 9(376), eaaf9655;

Eppinga, H., Weiland, C. J. S., Thio, H. B., van der Woude, C. J., Nijsten, T. E., Peppelenbosch, M. P., & Konstantinov, S. R. (2016). Similar depletion of protective Faecalibacterium prausnitzii in psoriasis and inflammatory bowel disease, but not in Hidradenitis suppurativa. Journal of Crohn’s and Colitis, 10(9), 1067-1075;

Scher, J. U., Sczesnak, A., Longman, R. S., Segata, N., Ubeda, C., Bielski, C., … Littman, D. R. (2013). Expansion of intestinal Prevotella copri correlates with enhanced susceptibility to arthritis. eLife, 2, e01202.

Maeda, Y., Kurakawa, T., Umemoto, E., Motooka, D., Ito, Y., Gotoh, K., … & Sakaguchi, N. (2016). Dysbiosis contributes to arthritis development via activation of autoreactive T cells in the intestine. Arthritis & Rheumatology, 68(11), 2646-2661.

Chen, J., Wright, K., Davis, J. M., Jeraldo, P., Marietta, E. V., Murray, J., … & Taneja, V. (2016). An expansion of rare lineage intestinal microbes characterizes rheumatoid arthritis. Genome medicine, 8(1), 43.

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