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4. Comprehensive Association Analyses of Extraintestinal Manifestations in Inflammatory Bowel Disease

Author

Khrom, Michelle, Long, Millie, Dube, Shishir, Robbins, Lori, Botwin, Gregory J., Yang, Shaohong, Mengesha, Emebet, Li, Dalin, Naito, Takeo, Bonthala, Nirupama N., Ha, Christina, Melmed, Gil, Rabizadeh, Shervin, Syal, Gaurav, Vasiliauskas, Eric, Ziring, David, Brant, Steven R., Cho, Judy, Duerr, Richard H., Rioux, John, Schumm, Phil, Silverberg, Mark, Ananthakrishnan, Ashwin N., Faubion, William A., Jabri, Bana, Lira, Sergio A., Newberry, Rodney D., Sandler, Robert S., Xavier, Ramnik J., Kugathasan, Subra, Hercules, David, Targan, Stephan R., Sartor, R. Balfour, Haritunians, Talin, and McGovern, Dermot P.B.

Published
2024
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7. Antigen-driven colonic inflammation is associated with development of dysplasia in primary sclerosing cholangitis

Author

Shaw, Dustin G., Aguirre-Gamboa, Raúl, Vieira, Marcos C., Gona, Saideep, DiNardi, Nicholas, Wang, Anni, Dumaine, Anne, Gelderloos-Arends, Jody, Earley, Zachary M., Meckel, Katherine R., Ciszewski, Cezary, Castillo, Anabella, Monroe, Kelly, Torres, Joana, Shah, Shailja C., Colombel, Jean-Frédéric, Itzkowitz, Steven, Newberry, Rodney, Cohen, Russell D., Rubin, David T., Quince, Christopher, Cobey, Sarah, Jonkers, Iris H., Weber, Christopher R., Pekow, Joel, Wilson, Patrick C., Barreiro, Luis B., and Jabri, Bana

Published
2023
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8. Fecal microbiota transplant rescues mice from human pathogen mediated sepsis by restoring systemic immunity

Author

Kim, Sangman M, DeFazio, Jennifer R, Hyoju, Sanjiv K, Sangani, Kishan, Keskey, Robert, Krezalek, Monika A, Khodarev, Nikolai N, Sangwan, Naseer, Christley, Scott, Harris, Katharine G, Malik, Ankit, Zaborin, Alexander, Bouziat, Romain, Ranoa, Diana R, Wiegerinck, Mara, Ernest, Jordan D, Shakhsheer, Baddr A, Fleming, Irma D, Weichselbaum, Ralph R, Antonopoulos, Dionysios A, Gilbert, Jack A, Barreiro, Luis B, Zaborina, Olga, Jabri, Bana, and Alverdy, John C

Subjects
Sepsis, Transplantation, Hematology, Infectious Diseases, Emerging Infectious Diseases, 5.1 Pharmaceuticals, Development of treatments and therapeutic interventions, Infection, Inflammatory and immune system, Good Health and Well Being, Animals, Butyric Acid, Fecal Microbiota Transplantation, Feces, Gastrointestinal Microbiome, Gastrointestinal Tract, Histone Deacetylase Inhibitors, Humans, Immunity, Interferon Regulatory Factor-3, Male, Mice, Inbred C57BL, Signal Transduction, Transcription, Genetic
Abstract

Death due to sepsis remains a persistent threat to critically ill patients confined to the intensive care unit and is characterized by colonization with multi-drug-resistant healthcare-associated pathogens. Here we report that sepsis in mice caused by a defined four-member pathogen community isolated from a patient with lethal sepsis is associated with the systemic suppression of key elements of the host transcriptome required for pathogen clearance and decreased butyrate expression. More specifically, these pathogens directly suppress interferon regulatory factor 3. Fecal microbiota transplant (FMT) reverses the course of otherwise lethal sepsis by enhancing pathogen clearance via the restoration of host immunity in an interferon regulatory factor 3-dependent manner. This protective effect is linked to the expansion of butyrate-producing Bacteroidetes. Taken together these results suggest that fecal microbiota transplantation may be a treatment option in sepsis associated with immunosuppression.

Published
2020

10. The gut protist Tritrichomonas arnold restrains virus-mediated loss of oral tolerance by modulating dietary antigen-presenting dendritic cells

Author

Medina Sanchez, Luzmariel, Siller, Magdalena, Zeng, Yanlin, Brigleb, Pamela H., Sangani, Kishan A., Soto, Ariadna S., Engl, Clarisse, Laughlin, Colin R., Rana, Mohit, Van Der Kraak, Lauren, Pandey, Surya P., Bender, Mackenzie J., Fitzgerald, Britney, Hedden, Lee, Fiske, Kay, Taylor, Gwen M., Wright, Austin P., Mehta, Isha D., Rahman, Syed A., Galipeau, Heather J., Mullett, Steven J., Gelhaus, Stacy L., Watkins, Simon C., Bercik, Premysl, Nice, Timothy J., Jabri, Bana, Meisel, Marlies, Das, Jishnu, Dermody, Terence S., Verdú, Elena F., and Hinterleitner, Reinhard

Published
2023
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14. A multilayered immune system through the lens of unconventional T cells

Author

Mayassi, Toufic, Barreiro, Luis B., Rossjohn, Jamie, and Jabri, Bana

Subjects
T cells -- Physiological aspects -- Natural history, Immune system -- Observations, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

The unconventional T cell compartment encompasses a variety of cell subsets that straddle the line between innate and adaptive immunity, often reside at mucosal surfaces and can recognize a wide range of non-polymorphic ligands. Recent advances have highlighted the role of unconventional T cells in tissue homeostasis and disease. In this Review, we recast unconventional T cell subsets according to the class of ligand that they recognize; their expression of semi-invariant or diverse T cell receptors; the structural features that underlie ligand recognition; their acquisition of effector functions in the thymus or periphery; and their distinct functional properties. Unconventional T cells follow specific selection rules and are poised to recognize self or evolutionarily conserved microbial antigens. We discuss these features from an evolutionary perspective to provide insights into the development and function of unconventional T cells. Finally, we elaborate on the functional redundancy of unconventional T cells and their relationship to subsets of innate and adaptive lymphoid cells, and propose that the unconventional T cell compartment has a critical role in our survival by expanding and complementing the role of the conventional T cell compartment in protective immunity, tissue healing and barrier function. This Review provides an overview of our current understanding of the unconventional T cell compartment and discusses the development and function of unconventional T cells from an evolutionary perspective., Author(s): Toufic Mayassi [sup.1] [sup.2] , Luis B. Barreiro [sup.2] [sup.3] [sup.4] , Jamie Rossjohn [sup.5] [sup.6] [sup.7] , Bana Jabri [sup.2] [sup.8] [sup.9] [sup.10] Author Affiliations: (1) Broad Institute [...]

Published
2021
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16. Safety and efficacy of AMG 714 in patients with type 2 refractory coeliac disease: a phase 2a, randomised, double-blind, placebo-controlled, parallel-group study

Author

Jabri, Bana, Murray, Joseph, DiMarino, Anthony, Kelly, Ciaran P, Byrnes, Valerie, Sanders, David, Lundin, Knut EA, Schumann, Michael, Bontkes, Hetty, Meresse, Bertrand, Roy Ariño, Garbiñe, Bhagat, Govind, Viiri, Keijo, Rounioja, Samuli, Bui, Jack, Perez Maseda, Raquel, García-Hoz, Carlota, Trinquand, Amelie, Vlad, George, Hadjivassiliou, Marios, Azizi, Michel, Blanchard, Anne, Llewellyn, Beth, Palmer, Ashleigh, Raymond, Ralph, Cellier, Christophe, Bouma, Gerd, van Gils, Tom, Khater, Sherine, Malamut, Georgia, Crespo, Laura, Collin, Pekka, Green, Peter H R, Crowe, Sheila E, Tsuji, Wayne, Butz, Eric, Cerf-Bensussan, Nadine, Macintyre, Elizabeth, Parnes, Jane R, Leon, Francisco, Hermine, Olivier, and Mulder, Chris J

Published
2019
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17. IL-15, gluten and HLA-DQ8 drive tissue destruction in coeliac disease

Author

Abadie, Valérie, Kim, Sangman M., Lejeune, Thomas, Palanski, Brad A., Ernest, Jordan D., Tastet, Olivier, Voisine, Jordan, Discepolo, Valentina, Marietta, Eric V., Hawash, Mohamed B. F., Ciszewski, Cezary, Bouziat, Romain, Panigrahi, Kaushik, Horwath, Irina, Zurenski, Matthew A., Lawrence, Ian, Dumaine, Anne, Yotova, Vania, Grenier, Jean-Christophe, Murray, Joseph A., Khosla, Chaitan, Barreiro, Luis B., and Jabri, Bana

Published
2020
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19. Human NKG2E Is Expressed and Forms an Intracytoplasmic Complex with CD94 and DAP12

Author

Orbelyan, Gerasim A, Tang, Fangming, Sally, Benjamin, Solus, Jason, Meresse, Bertrand, Ciszewski, Cezary, Grenier, Jean-Christophe, Barreiro, Luis B, Lanier, Lewis L, and Jabri, Bana

Subjects
Aetiology, 1.1 Normal biological development and functioning, Underpinning research, 2.1 Biological and endogenous factors, Adaptor Proteins, Signal Transducing, Amino Acid Sequence, Amino Acids, Animals, Binding Sites, Blotting, Western, Cell Line, Cytoplasm, Endoplasmic Reticulum, HEK293 Cells, Humans, Hydrophobic and Hydrophilic Interactions, Membrane Proteins, Microscopy, Confocal, Molecular Sequence Data, Mutation, NK Cell Lectin-Like Receptor Subfamily C, NK Cell Lectin-Like Receptor Subfamily D, Phylogeny, Protein Binding, Sequence Homology, Amino Acid, Immunology
Abstract

The NKG2 family of NK receptors includes activating and inhibitory members. With the exception of the homodimer-forming NKG2D, NKG2 receptors recognize the nonclassical MHC class I molecule HLA-E, and they can be subdivided into two groups: those that associate with and signal through DAP12 to activate cells, and those that contain an ITIM motif to promote inhibition. The function of NKG2 family member NKG2E is unclear in humans, and its surface expression has never been conclusively established, largely because there is no Ab that binds specifically to NKG2E. Seeking to determine a role for this molecule, we chose to investigate its expression and ability to form complexes with intracellular signaling molecules. We found that NKG2E was capable of associating with CD94 and DAP12 but that the complex was retained intracellularly at the endoplasmic reticulum instead of being expressed on cell surfaces, and that this localization was dependent on a sequence of hydrophobic amino acids in the extracellular domain of NKG2E. Because this particular sequence has emerged and been conserved selectively among higher order primates evolutionarily, this observation raises the intriguing possibility that NKG2E may function as an intracellular protein.

Published
2014

20. Microbes with higher metabolic independence are enriched in human gut microbiomes under stress

Author

Veseli, Iva, primary, Chen, Yiqun T., additional, Schechter, Matthew S., additional, Vanni, Chiara, additional, Fogarty, Emily C., additional, Watson, Andrea R., additional, Jabri, Bana, additional, Blekhman, Ran, additional, Willis, Amy D., additional, Yu, Michael K., additional, Fernàndez-Guerra, Antonio, additional, Füssel, Jessika, additional, and Eren, A. Murat, additional

Published
2023
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24. Dietary-fat-induced taurocholic acid promotes pathobiont expansion and colitis in Il10−/− mice

Author

Devkota, Suzanne, Wang, Yunwei, Musch, Mark W, Leone, Vanessa, Fehlner-Peach, Hannah, Nadimpalli, Anuradha, Antonopoulos, Dionysios A, Jabri, Bana, and Chang, Eugene B

Subjects
Biomedical and Clinical Sciences, Nutrition and Dietetics, Prevention, Nutrition, Digestive Diseases, Autoimmune Disease, Inflammatory Bowel Disease, 2.1 Biological and endogenous factors, Aetiology, Oral and gastrointestinal, Animals, Bile Acids and Salts, Bilophila, Colitis, Diet, Fat-Restricted, Dietary Fats, Inflammation, Inflammatory Bowel Diseases, Interleukin-10, Metagenome, Mice, Mice, Inbred C57BL, Milk, Molecular Sequence Data, Safflower Oil, Sulfites, Taurine, Taurocholic Acid, Th1 Cells, General Science & Technology
Abstract

The composite human microbiome of Western populations has probably changed over the past century, brought on by new environmental triggers that often have a negative impact on human health. Here we show that consumption of a diet high in saturated (milk-derived) fat, but not polyunsaturated (safflower oil) fat, changes the conditions for microbial assemblage and promotes the expansion of a low-abundance, sulphite-reducing pathobiont, Bilophila wadsworthia. This was associated with a pro-inflammatory T helper type 1 (T(H)1) immune response and increased incidence of colitis in genetically susceptible Il10(−/−), but not wild-type mice. These effects are mediated by milk-derived-fat-promoted taurine conjugation of hepatic bile acids, which increases the availability of organic sulphur used by sulphite-reducing microorganisms like B. wadsworthia. When mice were fed a low-fat diet supplemented with taurocholic acid, but not with glycocholic acid, for example, a bloom of B. wadsworthia and development of colitis were observed in Il10(−/−) mice. Together these data show that dietary fats, by promoting changes in host bile acid composition, can markedly alter conditions for gut microbial assemblage, resulting in dysbiosis that can perturb immune homeostasis. The data provide a plausible mechanistic basis by which Western-type diets high in certain saturated fats might increase the prevalence of complex immune-mediated diseases like inflammatory bowel disease in genetically susceptible hosts.

Published
2012

26. Reovirus infection triggers inflammatory responses to dietary antigens and development of celiac disease

Author

Bouziat, Romain, Hinterleitner, Reinhard, Brown, Judy J., Stencel-Baerenwald, Jennifer E., Ikizler, Mine, Mayassi, Toufic, Meisel, Marlies, Kim, Sangman M., Discepolo, Valentina, Pruijssers, Andrea J., Ernest, Jordan D., Iskarpatyoti, Jason A., Costes, Léa M. M., Lawrence, Ian, Palanski, Brad A., Varma, Mukund, Zurenski, Matthew A., Khomandiak, Solomiia, McAllister, Nicole, Aravamudhan, Pavithra, Boehme, Karl W., Hu, Fengling, Samsom, Janneke N., Reinecker, Hans-Christian, Kupfer, Sonia S., Guandalini, Stefano, Semrad, Carol E., Abadie, Valérie, Khosla, Chaitan, Barreiro, Luis B., Xavier, Ramnik J., Ng, Aylwin, Dermody, Terence S., and Jabri, Bana

Published
2017

27. Epitope-specific immunotherapy targeting CD4-positive T cells in coeliac disease: two randomised, double-blind, placebo-controlled phase 1 studies

Author

Goel, Gautam, King, Tim, Daveson, A James, Andrews, Jane M, Krishnarajah, Janakan, Krause, Richard, Brown, Gregor J E, Fogel, Ronald, Barish, Charles F, Epstein, Roger, Kinney, Timothy P, Miner, Philip B, Jr, Tye-Din, Jason A, Girardin, Adam, Taavela, Juha, Popp, Alina, Sidney, John, Mäki, Markku, Goldstein, Kaela E, Griffin, Patrick H, Wang, Suyue, Dzuris, John L, Williams, Leslie J, Sette, Alessandro, Xavier, Ramnik J, Sollid, Ludvig M, Jabri, Bana, and Anderson, Robert P

Published
2017
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28. Reprogramming of CTLs into natural killer-like cells in celiac disease

Author

Meresse, Bertrand, Curran, Shane A, Ciszewski, Cezary, Orbelyan, Gerasim, Setty, Mala, Bhagat, Govind, Lee, Leanne, Tretiakova, Maria, Semrad, Carol, Kistner, Emily, Winchester, Robert J, Braud, Veronique, Lanier, Lewis L, Geraghty, Daniel E, Green, Peter H, Guandalini, Stefano, and Jabri, Bana

Abstract

Celiac disease is an intestinal inflammatory disorder induced by dietary gluten in genetically susceptible individuals. The mechanisms underlying the massive expansion of interferon gamma-producing intraepithelial cytotoxic T lymphocytes (CTLs) and the destruction of the epithelial cells lining the small intestine of celiac patients have remained elusive. We report massive oligoclonal expansions of intraepithelial CTLs that exhibit a profound genetic reprogramming of natural killer (NK) functions. These CTLs aberrantly expressed cytolytic NK lineage receptors, such as NKG2C, NKp44, and NKp46, which associate with adaptor molecules bearing immunoreceptor tyrosine-based activation motifs and induce ZAP-70 phosphorylation, cytokine secretion, and proliferation independently of T cell receptor signaling. This NK transformation of CTLs may underlie both the self-perpetuating, gluten-independent tissue damage and the uncontrolled CTL expansion leading to malignant lymphomas in severe forms of celiac disease. Because similar changes were detected in a subset of CTLs from cytomegalovirus-seropositive patients, we suggest that a stepwise transformation of CTLs into NK-like cells may underlie immunopathology in various chronic infectious and inflammatory diseases.

Published
2006

30. Microbial signals drive pre-leukaemic myeloproliferation in a Tet2-deficient host

Author

Meisel, Marlies, Hinterleitner, Reinhard, Pacis, Alain, Chen, Li, Earley, Zachary M., Mayassi, Toufic, Pierre, Joseph F., Ernest, Jordan D., Galipeau, Heather J., Thuille, Nikolaus, Bouziat, Romain, Buscarlet, Manuel, Ringus, Daina L., Wang, Yitang, Li, Ye, Dinh, Vu, Kim, Sangman M., McDonald, Benjamin D., Zurenski, Matthew A., Musch, Mark W., Furtado, Glaucia C., Lira, Sergio A., Baier, Gottfried, Chang, Eugene B., Eren, A. Murat, Weber, Christopher R., Busque, Lambert, Godley, Lucy A., Verdú, Elena F., Barreiro, Luis B., and Jabri, Bana

Published
2018
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34. Maternal immune regulation of lactogenesis

Author

Corral, Dan, primary, Chi, Liang, additional, Gine, Eduard, additional, Yong, Daniel, additional, Nie, Jia, additional, Sun, Lilian, additional, Bhandoola, Avinash, additional, Bosselut, Remy, additional, Jabri, Bana, additional, and Belkaid, Yasmine, additional

Published
2023
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45. Microbes with higher metabolic independence are enriched in human gut microbiomes under stress

Author

Veseli, Iva, Chen, Yiqun T, Schechter, Matthew S, Vanni, Chiara, Fogarty, Emily C, Watson, Andrea R, Jabri, Bana, Blekhman, Ran, Willis, Amy D, Yu, Michael K, Fernàndez-Guerra, Antonio, Füssel, Jessika, Eren, A Murat, Veseli, Iva, Chen, Yiqun T, Schechter, Matthew S, Vanni, Chiara, Fogarty, Emily C, Watson, Andrea R, Jabri, Bana, Blekhman, Ran, Willis, Amy D, Yu, Michael K, Fernàndez-Guerra, Antonio, Füssel, Jessika, and Eren, A Murat

Abstract

A wide variety of human diseases are associated with loss of microbial diversity in the human gut, inspiring a great interest in the diagnostic or therapeutic potential of the microbiota. However, the ecological forces that drive diversity reduction in disease states remain unclear, rendering it difficult to ascertain the role of the microbiota in disease emergence or severity. One hypothesis to explain this phenomenon is that microbial diversity is diminished as disease states select for microbial populations that are more fit to survive environmental stress caused by inflammation or other host factors. Here, we tested this hypothesis on a large scale, by developing a software framework to quantify the enrichment of microbial metabolisms in complex metagenomes as a function of microbial diversity. We applied this framework to over 400 gut metagenomes from individuals who are healthy or diagnosed with inflammatory bowel disease (IBD). We found that high metabolic independence (HMI) is a distinguishing characteristic of microbial communities associated with individuals diagnosed with IBD. A classifier we trained using the normalized copy numbers of 33 HMI-associated metabolic modules not only distinguished states of health versus IBD, but also tracked the recovery of the gut microbiome following antibiotic treatment, suggesting that HMI is a hallmark of microbial communities in stressed gut environments.

Published
2023

46. Microbial-enrichment method enables high-throughput metagenomic characterization from host-rich samples

Author

Wu-Woods, Natalie J, Barlow, Jacob T, Trigodet, Florian, Shaw, Dustin G, Romano, Anna E, Jabri, Bana, Eren, A Murat, Ismagilov, Rustem F, Wu-Woods, Natalie J, Barlow, Jacob T, Trigodet, Florian, Shaw, Dustin G, Romano, Anna E, Jabri, Bana, Eren, A Murat, and Ismagilov, Rustem F

Abstract

Host–microbe interactions have been linked to health and disease states through the use of microbial taxonomic profiling, mostly via 16S ribosomal RNA gene sequencing. However, many mechanistic insights remain elusive, in part because studying the genomes of microbes associated with mammalian tissue is difficult due to the high ratio of host to microbial DNA in such samples. Here we describe a microbial-enrichment method (MEM), which we demonstrate on a wide range of sample types, including saliva, stool, intestinal scrapings, and intestinal mucosal biopsies. MEM enabled high-throughput characterization of microbial metagenomes from human intestinal biopsies by reducing host DNA more than 1,000-fold with minimal microbial community changes (roughly 90% of taxa had no significant differences between MEM-treated and untreated control groups). Shotgun sequencing of MEM-treated human intestinal biopsies enabled characterization of both high- and low-abundance microbial taxa, pathways and genes longitudinally along the gastrointestinal tract. We report the construction of metagenome-assembled genomes directly from human intestinal biopsies for bacteria and archaea at relative abundances as low as 1%. Analysis of metagenome-assembled genomes reveals distinct subpopulation structures between the small and large intestine for some taxa. MEM opens a path for the microbiome field to acquire deeper insights into host–microbe interactions by enabling in-depth characterization of host-tissue-associated microbial communities.

Published
2023

47. Metabolic independence drives gut microbial colonization and resilience in health and disease

Author

Watson, Andrea R, Füssel, Jessika, Veseli, Iva, DeLongchamp, Johanna Zaal, Silva, Marisela, Trigodet, Florian, Lolans, Karen, Shaiber, Alon, Fogarty, Emily, Runde, Joseph M, Quince, Christopher, Yu, Michael K, Söylev, Arda, Morrison, Hilary G, Lee, Sonny TM, Kao, Dina, Rubin, David T, Jabri, Bana, Louie, Thomas, Eren, A Murat, Watson, Andrea R, Füssel, Jessika, Veseli, Iva, DeLongchamp, Johanna Zaal, Silva, Marisela, Trigodet, Florian, Lolans, Karen, Shaiber, Alon, Fogarty, Emily, Runde, Joseph M, Quince, Christopher, Yu, Michael K, Söylev, Arda, Morrison, Hilary G, Lee, Sonny TM, Kao, Dina, Rubin, David T, Jabri, Bana, Louie, Thomas, and Eren, A Murat

Abstract

Background: Changes in microbial community composition as a function of human health and disease states have sparked remarkable interest in the human gut microbiome. However, establishing reproducible insights into the determinants of microbial succession in disease has been a formidable challenge. Results: Here we use fecal microbiota transplantation (FMT) as an in natura experimental model to investigate the association between metabolic independence and resilience in stressed gut environments. Our genome-resolved metagenomics survey suggests that FMT serves as an environmental filter that favors populations with higher metabolic independence, the genomes of which encode complete metabolic modules to synthesize critical metabolites, including amino acids, nucleotides, and vitamins. Interestingly, we observe higher completion of the same biosynthetic pathways in microbes enriched in IBD patients. Conclusions: These observations suggest a general mechanism that underlies changes in diversity in perturbed gut environments and reveal taxon-independent markers of “dysbiosis” that may explain why widespread yet typically low-abundance members of healthy gut microbiomes can dominate under inflammatory conditions without any causal association with disease.

Published
2023

48. Duodenal bacterial proteolytic activity determines sensitivity to dietary antigen through protease-activated receptor-2

Author

Caminero, Alberto, McCarville, Justin L., Galipeau, Heather J., Deraison, Celine, Bernier, Steve P., Constante, Marco, Rolland, Corinne, Meisel, Marlies, Murray, Joseph A., Yu, Xuechen B., Alaedini, Armin, Coombes, Brian K., Bercik, Premysl, Southward, Carolyn M., Ruf, Wolfram, Jabri, Bana, Chirdo, Fernando G., Casqueiro, Javier, Surette, Michael G., Vergnolle, Nathalie, and Verdu, Elena F.

Published
2019
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49. Genetic coding variant in complement factor B (CFB) is associated with increased risk for perianal Crohn's disease and leads to impaired CFB cleavage and phagocytosis.

Author

Akhlaghpour, Marzieh, Haritunians, Talin, More, Shyam K., Thomas, Lisa S., Stamps, Dalton T., Dube, Shishir, Dalin Li, Shaohong Yang, Landers, Carol J., Mengesha, Emebet, Hamade, Hussein, Murali, Ramachandran, Potdar, Alka A., Wolf, Andrea J., Botwin, Gregory J., Khrom, Michelle, Ananthakrishnan, Ashwin N., Faubion, William A., Jabri, Bana, and Lira, Sergio A.

Subjects
CROHN'S disease, GENETIC variation, PHAGOCYTOSIS, GENETIC code, MEDICAL sciences, PULMONARY alveolar proteinosis, CHOLANGITIS
Published
2023
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50. Inflammation in the proximal colon is a risk factor for the development of colorectal neoplasia in inflammatory bowel disease patients with primary sclerosing cholangitis.

Author

Jamil, Omar K., Shaw, Dustin, Deng, Zifeng, Dinardi, Nicholas, Fillman, Natalie, Khanna, Shivani, Krugliak Cleveland, Noa, Sakuraba, Atsushi, Weber, Christopher R., Cohen, Russell D., Dalal, Sushila, Jabri, Bana, Rubin, David T., and Pekow, Joel

Subjects
INFLAMMATORY bowel diseases, CHOLANGITIS, DISEASE risk factors, COLON (Anatomy), INFLAMMATION, TUMORS
Abstract

Background: Patients with primary sclerosing cholangitis (PSC) and inflammatory bowel disease (IBD) have an increased risk of developing colorectal neoplasia (CRN) in the proximal colon. Objectives: To evaluate whether duration and severity of inflammation are linked to the development of CRN in this population. Design: Retrospective, case–control chart review of patients with PSC and IBD at a tertiary care center. Methods: Disease activity was scored per colonic segment at each colonoscopy prior to the first instance of observed CRN using a modified Mayo endoscopic sub-score and histologic assessment. Patients in the CRN-positive group were compared to controls that did not. Results: In all, 72 PSC-IBD patients with no history of CRN were identified, 13 of whom developed CRN after at least one colonoscopy at our institution. Patients in the CRN-positive group had significantly more endoscopic (p < 0.01) and histologic (p < 0.01) inflammation in the right compared to the control group prior to the development of dysplasia. There was significantly greater endoscopic inflammation in the segment of the colon with a dysplastic lesion than other segments of the colon (p = 0.018). Patients with moderate/severe lifetime endoscopic (p = 0.02) or histologic inflammation (p = 0.04) score had a lower probability of remaining free of dysplasia during follow-up. Nearly half of the patients with dysplasia had invisible lesions found on random biopsy. Conclusions: Endoscopic and histologic inflammation in the proximal colon are risk factors for CRN in patients with PSC-IBD. PSC-IBD patients frequently have subclinical inflammation, and these findings support the practice of regular assessment of disease activity and random biopsy of inflamed and uninflamed areas in patients with PSC with the goal of reducing inflammation to prevent the development of CRN. Plain language summary: Patients with PSC and IBD have not been examined as a cohort to assess for risk factors for CRN. We found that severe inflammation in the proximal colon is the main risk factor for CRN in these patients. [ABSTRACT FROM AUTHOR]

Published
2023
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