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2. Microclimate is a strong predictor of the native and invasive plant‐associated soil microbiome on San Cristóbal Island, Galápagos archipelago

Author

Schoenborn, Alexi A., primary, Yannarell, Sarah M., additional, MacVicar, Caroline T., additional, Barriga‐Medina, Noelia N., additional, Bonham, Kevin S., additional, Leon‐Reyes, Antonio, additional, Riveros‐Iregui, Diego, additional, Klepac‐Ceraj, Vanja, additional, and Shank, Elizabeth A., additional

Published
2023
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3. Agr2-associated ER stress promotes adherent-invasive E. coli dysbiosis and triggers CD103+ dendritic cell IL-23-dependent ileocolitis

Author

Viladomiu, Monica, primary, Khounlotham, Manirath, additional, Dogan, Belgin, additional, Lima, Svetlana F., additional, Elsaadi, Ahmed, additional, Cardakli, Emre, additional, Castellanos, Jim G., additional, Ng, Charles, additional, Herzog, Jeremy, additional, Schoenborn, Alexi A., additional, Ellermann, Melissa, additional, Liu, Bo, additional, Zhang, Shiying, additional, Gulati, Ajay S., additional, Sartor, R. Balfour, additional, Simpson, Kenneth W., additional, Lipkin, Steven M., additional, and Longman, Randy S., additional

Published
2022
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5. Microclimate is a strong predictor of the native and invasive plant-associated soil microbiota on San Cristóbal Island, Galápagos archipelago

Author

Schoenborn, Alexi A., primary, Yannarell, Sarah M., additional, MacVicar, Caroline T., additional, Barriga-Medina, Noelia N., additional, Markillie, Meng, additional, Mitchell, Hugh, additional, Bonham, Kevin S., additional, Leon-Reyes, Antonio, additional, Riveros-Iregui, Diego, additional, Klepac-Ceraj, Vanja, additional, and Shank, Elizabeth A., additional

Published
2022
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6. ADHERENT-INVASIVE E. COLI PROMOTE ER STRESS TO SUPPORT IL23R-DRIVEN AGR2-DEPENDENT ILEOCOLITIS

Author

Viladomiu, Monica, primary, Khounlotham, Manirath, additional, Dogan, Belgin, additional, Lima, Svetlana, additional, Elsaadi, Ahmed, additional, Herzog, Jeremy, additional, Schoenborn, Alexi, additional, Ellermann, Melissa, additional, Liu, Bo, additional, Zhang, Shiying, additional, Gulati, Ajay, additional, Sartor, R. Balfour, additional, Simpson, Kenneth, additional, Lipkin, Steve, additional, and Longman, Randy, additional

Published
2022
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7. ADHERENT-INVASIVEE. COLI PROMOTE ER STRESS TO SUPPORT IL23R-DRIVEN AGR2-DEPENDENT ILEOCOLITIS

Author

Viladomiu, Monica, primary, Khounlotham, Manirath, additional, Dogan, Belgin, additional, Lima, Svetlana, additional, Elsaadi, Ahmed, additional, Herzog, Jeremy, additional, Schoenborn, Alexi, additional, Ellermann, Melissa, additional, Liu, Bo, additional, Zhang, Shiying, additional, Gulati, Ajay, additional, Sartor, R Balfour, additional, Simpson, Kenneth, additional, Lipkin, Steve, additional, and Longman, Randy, additional

Published
2022
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11. Irgm1-deficiency leads to myeloid dysfunction in colon lamina propria and susceptibility to the intestinal pathogen Citrobacter rodentium

Author

Taylor, Gregory A., primary, Huang, Hsin-I, additional, Fee, Brian E., additional, Youssef, Nourhan, additional, Jewell, Mark L., additional, Cantillana, Viviana, additional, Schoenborn, Alexi A., additional, Rogala, Allison R., additional, Buckley, Anne F., additional, Feng, Carl G., additional, Vallance, Bruce A., additional, Gulati, Ajay S., additional, and Hammer, Gianna E., additional

Published
2020
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12. Irgm1-deficiency leads to myeloid dysfunction in colon lamina propria and susceptibility to the intestinal pathogenCitrobacter rodentium

Author

Taylor, Gregory A., primary, Huang, Hsin-I, additional, Fee, Brian E., additional, Yousssef, Nourhan, additional, Cantillana, Viviana, additional, Schoenborn, Alexi A., additional, Rogala, Allison R., additional, Buckley, Anne F., additional, Vallance, Bruce A., additional, Gulati, Ajay S., additional, and Hammer, Gianna E., additional

Published
2019
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15. Environmental factors regulate Paneth cell phenotype and host susceptibility to intestinal inflammation in Irgm1-deficient mice

Author

Rogala, Allison R., primary, Schoenborn, Alexi A., additional, Fee, Brian E., additional, Cantillana, Viviana A., additional, Joyce, Maria J., additional, Gharaibeh, Raad Z., additional, Roy, Sayanty, additional, Fodor, Anthony A., additional, Sartor, R. Balfour, additional, Taylor, Gregory A., additional, and Gulati, Ajay S., additional

Published
2017
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16. Akkermansia muciniphila mediates negative effects of IFNγ on glucose metabolism

Author

Greer, Renee L., primary, Dong, Xiaoxi, additional, Moraes, Ana Carolina F., additional, Zielke, Ryszard A., additional, Fernandes, Gabriel R., additional, Peremyslova, Ekaterina, additional, Vasquez-Perez, Stephany, additional, Schoenborn, Alexi A., additional, Gomes, Everton P., additional, Pereira, Alexandre C., additional, Ferreira, Sandra R. G., additional, Yao, Michael, additional, Fuss, Ivan J., additional, Strober, Warren, additional, Sikora, Aleksandra E., additional, Taylor, Gregory A., additional, Gulati, Ajay S., additional, Morgun, Andrey, additional, and Shulzhenko, Natalia, additional

Published
2016
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19. Collecting Biospecimens From an Internet-Based Prospective Cohort Study of Inflammatory Bowel Disease (CCFA Partners): A Feasibility Study

Author

Randell, Rachel L, primary, Gulati, Ajay S, additional, Cook, Suzanne F, additional, Martin, Christopher F, additional, Chen, Wenli, additional, Jaeger, Elizabeth L, additional, Schoenborn, Alexi A, additional, Basta, Patricia V, additional, Dejong, Hendrik, additional, Luo, Jingchun, additional, Gallant, Marisa, additional, Sandler, Robert S, additional, Long, Millie D, additional, and Kappelman, Michael D, additional

Published
2016
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20. Inflammation-Induced Acid Tolerance Genes gadAB in Luminal Commensal Escherichia coli Attenuate Experimental Colitis

Author

Gulati, Ajay S., Tchaptchet, Sandrine, Schoenborn, Alexi, Hansen, Jonathan J., Goeser, Laura, Sartor, R. Balfour, and Fan, Ting-Jia

Abstract

Dysregulated immune responses to commensal intestinal bacteria, including Escherichia coli , contribute to the development of inflammatory bowel diseases (IBDs) and experimental colitis. Reciprocally, E. coli responds to chronic intestinal inflammation by upregulating expression of stress response genes, including gadA and gadB . GadAB encode glutamate decarboxylase and protect E. coli from the toxic effects of low pH and fermentation acids, factors present in the intestinal lumen in patients with active IBDs. We hypothesized that E. coli upregulates gadAB during inflammation to enhance its survival and virulence. Using real-time PCR, we determined gadAB expression in luminal E. coli from ex-germfree wild-type (WT) and interleukin-10 (IL-10) knockout (KO) (IL-10 −/− ) mice selectively colonized with a commensal E. coli isolate (NC101) that causes colitis in KO mice in isolation or in combination with 7 other commensal intestinal bacterial strains. E. coli survival and host inflammatory responses were measured in WT and KO mice colonized with NC101 or a mutant lacking the gadAB genes (NC101Δ gadAB ). The susceptibility of NC101 and NC101Δ gadAB to killing by host antimicrobial peptides and their translocation across intestinal epithelial cells were evaluated using bacterial killing assays and transwell experiments, respectively. We show that expression of gadAB in luminal E. coli increases proportionately with intestinal inflammation in KO mice and enhances the susceptibility of NC101 to killing by the host antimicrobial peptide cryptdin-4 but decreases bacterial transmigration across intestinal epithelial cells, colonic inflammation, and mucosal immune responses. Chronic intestinal inflammation upregulates acid tolerance pathways in commensal E. coli isolates, which, contrary to our original hypothesis, limits their survival and colitogenic potential. Further investigation of microbial adaptation to immune-mediated inflammation may provide novel insights into the pathogenesis and treatment of IBDs.

Published
2013
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21. Su1318 Feasibility of Collecting Biospecimens From an Internet-Based Inflammatory Bowel Disease Cohort (CCFA Partners)

Author

Randell, Rachel L., primary, Cook, Suzanne, additional, Martin, Christopher F., additional, Chen, Wenli, additional, Goble, Lucy, additional, Jaeger, Elizabeth L., additional, Schoenborn, Alexi A., additional, Gulati, Ajay S., additional, Sandler, Robert S., additional, Long, Millie D., additional, and Kappelman, Michael, additional

Published
2015
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26. The Gene Desert Mammary Carcinoma Susceptibility Locus Mcs1a Regulates Nr2f1 Modifying Mammary Epithelial Cell Differentiation and Proliferation

Author

Smits, Bart M. G., primary, Haag, Jill D., additional, Rissman, Anna I., additional, Sharma, Deepak, additional, Tran, Ann, additional, Schoenborn, Alexi A., additional, Baird, Rachael C., additional, Peiffer, Dan S., additional, Leinweber, David Q., additional, Muelbl, Matthew J., additional, Meilahn, Amanda L., additional, Eichelberg, Mark R., additional, Leng, Ning, additional, Kendziorski, Christina, additional, John, Manorama C., additional, Powers, Patricia A., additional, Alexander, Caroline M., additional, and Gould, Michael N., additional

Published
2013
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28. Agr2-associated ER stress promotes adherent-invasive E. colidysbiosis and triggers CD103+dendritic cell IL-23-dependent ileocolitis

Author

Viladomiu, Monica, Khounlotham, Manirath, Dogan, Belgin, Lima, Svetlana F., Elsaadi, Ahmed, Cardakli, Emre, Castellanos, Jim G., Ng, Charles, Herzog, Jeremy, Schoenborn, Alexi A., Ellermann, Melissa, Liu, Bo, Zhang, Shiying, Gulati, Ajay S., Sartor, R. Balfour, Simpson, Kenneth W., Lipkin, Steven M., and Longman, Randy S.

Abstract

Endoplasmic reticulum (ER) stress is associated with Crohn’s disease (CD), but its impact on host-microbe interaction in disease pathogenesis is not well defined. Functional deficiency in the protein disulfide isomerase anterior gradient 2 (AGR2) has been linked with CD and leads to epithelial cell ER stress and ileocolitis in mice and humans. Here, we show that ileal expression of AGR2correlates with mucosal Enterobactericeaeabundance in human inflammatory bowel disease (IBD) and that Agr2deletion leads to ER-stress-dependent expansion of mucosal-associated adherent-invasive Escherichia coli(AIEC), which drives Th17 cell ileocolitis in mice. Mechanistically, our data reveal that AIEC-induced epithelial cell ER stress triggers CD103+dendritic cell production of interleukin-23 (IL-23) and that IL-23R is required for ileocolitis in Agr2−/−mice. Overall, these data reveal a specific and reciprocal interaction of the expansion of the CD pathobiont AIEC with ER-stress-associated ileocolitis and highlight a distinct cellular mechanism for IL-23-dependent ileocolitis.

Published
2022
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29. The Gene Desert Mammary Carcinoma Susceptibility Locus Mcs1a Regulates Nr2f1 Modifying Mammary Epithelial Cell Differentiation and Proliferation.

Author

Smits, Bart M. G., Haag, Jill D., Rissman, Anna I., Sharma, Deepak, Tran, Ann, Schoenborn, Alexi A., Baird, Rachael C., Peiffer, Dan S., Leinweber, David Q., Muelbl, Matthew J., Meilahn, Amanda L., Eichelberg, Mark R., Leng, Ning, Kendziorski, Christina, John, Manorama C., Powers, Patricia A., Alexander, Caroline M., and Gould, Michael N.

Subjects
BREAST cancer research, MAMMARY glands, GENE expression, CHROMOSOMES, STANDARD deviations
Abstract

Genome-wide association studies have revealed that many low-penetrance breast cancer susceptibility loci are located in non-protein coding genomic regions; however, few have been characterized. In a comparative genetics approach to model such loci in a rat breast cancer model, we previously identified the mammary carcinoma susceptibility locus Mcs1a. We now localize Mcs1a to a critical interval (277 Kb) within a gene desert. Mcs1a reduces mammary carcinoma multiplicity by 50% and acts in a mammary cell-autonomous manner. We developed a megadeletion mouse model, which lacks 535 Kb of sequence containing the Mcs1a ortholog. Global gene expression analysis by RNA-seq revealed that in the mouse mammary gland, the orphan nuclear receptor gene Nr2f1/Coup-tf1 is regulated by Mcs1a. In resistant Mcs1a congenic rats, as compared with susceptible congenic control rats, we found Nr2f1 transcript levels to be elevated in mammary gland, epithelial cells, and carcinoma samples. Chromatin looping over ∼820 Kb of sequence from the Nr2f1 promoter to a strongly conserved element within the Mcs1a critical interval was identified. This element contains a 14 bp indel polymorphism that affects a human-rat-mouse conserved COUP-TF binding motif and is a functional Mcs1a candidate. In both the rat and mouse models, higher Nr2f1 transcript levels are associated with higher abundance of luminal mammary epithelial cells. In both the mouse mammary gland and a human breast cancer global gene expression data set, we found Nr2f1 transcript levels to be strongly anti-correlated to a gene cluster enriched in cell cycle-related genes. We queried 12 large publicly available human breast cancer gene expression studies and found that the median NR2F1 transcript level is consistently lower in ‘triple-negative’ (ER-PR-HER2-) breast cancers as compared with ‘receptor-positive’ breast cancers. Our data suggest that the non-protein coding locus Mcs1a regulates Nr2f1, which is a candidate modifier of differentiation, proliferation, and mammary cancer risk. [ABSTRACT FROM AUTHOR]

Published
2013
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30. Inflammation-Induced Acid Tolerance Genes gadABin Luminal Commensal Escherichia coliAttenuate Experimental Colitis

Author

Tchaptchet, Sandrine, Fan, Ting-Jia, Goeser, Laura, Schoenborn, Alexi, Gulati, Ajay S., Sartor, R. Balfour, and Hansen, Jonathan J.

Abstract

ABSTRACTDysregulated immune responses to commensal intestinal bacteria, including Escherichia coli, contribute to the development of inflammatory bowel diseases (IBDs) and experimental colitis. Reciprocally, E. coliresponds to chronic intestinal inflammation by upregulating expression of stress response genes, including gadAand gadB. GadAB encode glutamate decarboxylase and protect E. colifrom the toxic effects of low pH and fermentation acids, factors present in the intestinal lumen in patients with active IBDs. We hypothesized that E. coliupregulates gadABduring inflammation to enhance its survival and virulence. Using real-time PCR, we determined gadABexpression in luminal E. colifrom ex-germfree wild-type (WT) and interleukin-10 (IL-10) knockout (KO) (IL-10-/-) mice selectively colonized with a commensal E. coliisolate (NC101) that causes colitis in KO mice in isolation or in combination with 7 other commensal intestinal bacterial strains. E. colisurvival and host inflammatory responses were measured in WT and KO mice colonized with NC101 or a mutant lacking the gadABgenes (NC101?gadAB). The susceptibility of NC101 and NC101?gadABto killing by host antimicrobial peptides and their translocation across intestinal epithelial cells were evaluated using bacterial killing assays and transwell experiments, respectively. We show that expression of gadABin luminal E. coliincreases proportionately with intestinal inflammation in KO mice and enhances the susceptibility of NC101 to killing by the host antimicrobial peptide cryptdin-4 but decreases bacterial transmigration across intestinal epithelial cells, colonic inflammation, and mucosal immune responses. Chronic intestinal inflammation upregulates acid tolerance pathways in commensal E. coliisolates, which, contrary to our original hypothesis, limits their survival and colitogenic potential. Further investigation of microbial adaptation to immune-mediated inflammation may provide novel insights into the pathogenesis and treatment of IBDs.

Published
2013
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32. Environmental factors regulate Paneth cell phenotype and host susceptibility to intestinal inflammation in Irgm1-deficient mice

Author

Rogala, Allison R., Schoenborn, Alexi A., Fee, Brian E., Cantillana, Viviana A., Joyce, Maria J., Gharaibeh, Raad Z., Roy, Sayanty, Fodor, Anthony A., Sartor, R. Balfour, Taylor, Gregory A., and Gulati, Ajay S.

Abstract

Crohn's disease (CD) represents a chronic inflammatory disorder of the intestinal tract. Several susceptibility genes have been linked to CD, though their precise role in the pathogenesis of this disorder remains unclear. Immunity-related GTPase M (IRGM) is an established risk allele in CD. We have shown previously that conventionally raised (CV) mice lacking the IRGM ortholog, Irgm1 exhibit abnormal Paneth cells (PCs) and increased susceptibility to intestinal injury. In the present study, we sought to utilize this model system to determine if environmental conditions impact these phenotypes, as is thought to be the case in human CD. To accomplish this, wild-type and Irgm1−/− mice were rederived into specific pathogen-free (SPF) and germ-free (GF) conditions. We next assessed how these differential housing environments influenced intestinal injury patterns, and epithelial cell morphology and function in wild-type and Irgm1−/− mice. Remarkably, in contrast to CV mice, SPF Irgm1−/− mice showed only a slight increase in susceptibility to dextran sodium sulfate-induced inflammation. SPF Irgm1−/− mice also displayed minimal abnormalities in PC number and morphology, and in antimicrobial peptide expression. Goblet cell numbers and epithelial proliferation were also unaffected by Irgm1 in SPF conditions. No microbial differences were observed between wild-type and Irgm1−/− mice, but gut bacterial communities differed profoundly between CV and SPF mice. Specifically, Helicobacter sequences were significantly increased in CV mice; however, inoculating SPF Irgm1−/− mice with Helicobacter hepaticus was not sufficient to transmit a pro-inflammatory phenotype. In summary, our findings suggest the impact of Irgm1-deficiency on susceptibility to intestinal inflammation and epithelial function is critically dependent on environmental influences. This work establishes the importance of Irgm1−/− mice as a model to elucidate host-environment interactions that regulate mucosal homeostasis and intestinal inflammatory responses. Defining such interactions will be essential for developing novel preventative and therapeutic strategies for human CD.

Published
2018
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33. Collecting Biospecimens From an Internet-Based Prospective Cohort Study of Inflammatory Bowel Disease (CCFA Partners): A Feasibility Study.

Author

Randell, Rachel L, Gulati, Ajay S, Cook, Suzanne F, Martin, Christopher F, Chen, Wenli, Jaeger, Elizabeth L, Schoenborn, Alexi A, Basta, Patricia V, Dejong, Hendrik, Luo, Jingchun, Gallant, Marisa, Sandler, Robert S, Long, Millie D, Kappelman, Michael D, and Randell, MD, Rachel L

Subjects
INFLAMMATORY bowel diseases, INTERNET in medicine, DIAGNOSTIC specimens, PHLEBOTOMY, POLYMERASE chain reaction
Abstract

Background: The Internet has successfully been used for patient-oriented survey research. Internet-based translational research may also be possible. Objective: Our aim was to study the feasibility of collecting biospecimens from CCFA Partners, an Internet-based inflammatory bowel disease (IBD) cohort. Methods: From August 20, 2013, to January 4, 2014, we randomly sampled 412 participants, plus 179 from a prior validation study, and invited them to contribute a biospecimen. Participants were randomized to type (blood, saliva), incentive (none, US $20, or US $50), and collection method for blood. The first 82 contributors were also invited to contribute stool. We used descriptive statistics and t tests for comparisons. Results: Of the 591 participants, 239 (40.4%) indicated interest and 171 (28.9%) contributed a biospecimen. Validation study participants were more likely to contribute than randomly selected participants (44% versus 23%, P<.001). The return rate for saliva was higher than blood collected by mobile phlebotomist and at doctors' offices (38%, 31%, and 17% respectively, P<.001). For saliva, incentives were associated with higher return rates (43-44% versus 26%, P=.04); 61% contributed stool. Fourteen IBD-associated single nucleotide polymorphisms were genotyped, and risk allele frequencies were comparable to other large IBD populations. Bacterial DNA was successfully extracted from stool samples and was of sufficient quality to permit quantitative polymerase chain reaction for total bacteria. Conclusions: Participants are willing to contribute and it is feasible to collect biospecimens from an Internet-based IBD cohort. Home saliva kits yielded the highest return rate, though mobile phlebotomy was also effective. All samples were sufficient for genetic testing. These data support the feasibility of developing a centralized collection of biospecimens from this cohort to facilitate IBD translational studies. [ABSTRACT FROM AUTHOR]

Published
2016
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34. Agr2-associated ER stress promotes adherent-invasive E. coli dysbiosis and triggers CD103 + dendritic cell IL-23-dependent ileocolitis.

Author

Viladomiu M, Khounlotham M, Dogan B, Lima SF, Elsaadi A, Cardakli E, Castellanos JG, Ng C, Herzog J, Schoenborn AA, Ellermann M, Liu B, Zhang S, Gulati AS, Sartor RB, Simpson KW, Lipkin SM, and Longman RS

Subjects
Animals, Humans, Mice, Dendritic Cells, Escherichia coli, Interleukin-23, Oncogene Proteins, Crohn Disease genetics, Crohn Disease microbiology, Dysbiosis, Mucoproteins genetics, Escherichia coli Infections
Abstract

Endoplasmic reticulum (ER) stress is associated with Crohn's disease (CD), but its impact on host-microbe interaction in disease pathogenesis is not well defined. Functional deficiency in the protein disulfide isomerase anterior gradient 2 (AGR2) has been linked with CD and leads to epithelial cell ER stress and ileocolitis in mice and humans. Here, we show that ileal expression of AGR2 correlates with mucosal Enterobactericeae abundance in human inflammatory bowel disease (IBD) and that Agr2 deletion leads to ER-stress-dependent expansion of mucosal-associated adherent-invasive Escherichia coli (AIEC), which drives Th17 cell ileocolitis in mice. Mechanistically, our data reveal that AIEC-induced epithelial cell ER stress triggers CD103 + dendritic cell production of interleukin-23 (IL-23) and that IL-23R is required for ileocolitis in Agr2 -/- mice. Overall, these data reveal a specific and reciprocal interaction of the expansion of the CD pathobiont AIEC with ER-stress-associated ileocolitis and highlight a distinct cellular mechanism for IL-23-dependent ileocolitis., Competing Interests: Declaration of interests The authors declare no competing interests., (Copyright © 2022 The Author(s). Published by Elsevier Inc. All rights reserved.)

Published
2022
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35. Irgm1-deficient mice exhibit Paneth cell abnormalities and increased susceptibility to acute intestinal inflammation.

Author

Liu B, Gulati AS, Cantillana V, Henry SC, Schmidt EA, Daniell X, Grossniklaus E, Schoenborn AA, Sartor RB, and Taylor GA

Subjects
Animals, Autophagy, Colitis metabolism, Dextran Sulfate toxicity, Female, GTP-Binding Proteins genetics, Gene Expression Regulation physiology, Ileitis chemically induced, Ileitis metabolism, Inflammation genetics, Inflammation metabolism, Male, Mice, Mice, Knockout, Mitophagy, Paneth Cells metabolism, Colitis chemically induced, GTP-Binding Proteins metabolism, Paneth Cells pathology
Abstract

Crohn's disease (CD) is a chronic, immune-mediated, inflammatory disorder of the intestine that has been linked to numerous susceptibility genes, including the immunity-related GTPase (IRG) M (IRGM). IRGs comprise a family of proteins known to confer resistance to intracellular infections through various mechanisms, including regulation of phagosome processing, cell motility, and autophagy. However, despite its association with CD, the role of IRGM and other IRGs in regulating intestinal inflammation is unclear. We investigated the involvement of Irgm1, an ortholog of IRGM, in the genesis of murine intestinal inflammation. After dextran sodium sulfate exposure, Irgm1-deficient [Irgm1 knockout (KO)] mice showed increased acute inflammation in the colon and ileum, with worsened clinical responses. Marked alterations of Paneth cell location and granule morphology were present in Irgm1 KO mice, even without dextran sodium sulfate exposure, and were associated with impaired mitophagy and autophagy in Irgm1 KO intestinal cells (including Paneth cells). This was manifested by frequent tubular and swollen mitochondria and increased LC3-positive autophagic structures. Interestingly, these LC3-positive structures often contained Paneth cell granules. These results suggest that Irgm1 modulates acute inflammatory responses in the mouse intestine, putatively through the regulation of gut autophagic processes, that may be pivotal for proper Paneth cell functioning.

Published
2013
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