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1. Metabolic immaturity and breastmilk bile acid metabolites are central determinants of heightened newborn vulnerability to norovirus diarrhea

Author

Peiper, Amy M., Morales Aparicio, Joyce, Hu, Zhengzheng, Phophi, Lufuno, Helm, Emily W., Rubinstein, Rebecca J., Phillips, Matthew, Williams, Caroline G., Subramanian, Saravanan, Cross, Michael, Iyer, Neha, Nguyen, Quyen, Newsome, Rachel, Jobin, Christian, Langel, Stephanie N., Bucardo, Filemon, Becker-Dreps, Sylvia, Tan, Xiao-Di, Dawson, Paul A., and Karst, Stephanie M.

Published
2024
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5. Modulating microbiome-immune axis in the deployment-related chronic diseases of Veterans: report of an expert meeting

Author

Sun, Jun, primary, Ince, M. Nedim, additional, Abraham, Clara, additional, Barrett, Terrence, additional, Brenner, Lisa A., additional, Cong, Yingzi, additional, Dashti, Reza, additional, Dudeja, Pradeep K., additional, Elliott, David, additional, Griffith, Thomas S., additional, Heeger, Peter S., additional, Hoisington, Andrew, additional, Irani, Kaikobad, additional, Kim, Tae Kon, additional, Kapur, Neeraj, additional, Leventhal, Joseph, additional, Mohamadzadeh, Mansour, additional, Mutlu, Ece, additional, Newberry, Rodney, additional, Peled, Jonathan U., additional, Rubinstein, Israel, additional, Sengsayadeth, Salyka, additional, Tan, Chen Sabrina, additional, Tan, Xiao-Di, additional, Tkaczyk, Eric, additional, Wertheim, Jason, additional, and Zhang, Zheng Jenny, additional

Published
2023
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8. B Cell Lymphocytosis in Juvenile Dermatomyositis

Author

Costin, Christopher, primary, Khojah, Amer, additional, Ochfeld, Elisa, additional, Morgan, Gabrielle, additional, Subramanian, Saravanan, additional, Klein-Gitelman, Marisa, additional, Tan, Xiao-Di, additional, and Pachman, Lauren M., additional

Published
2023
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12. LncRNA H19 Regulates Intestinal Serotonin Transporter (SERT) Expression

Author

Natarajan Anbazhagan, Arivarasu, primary, Frank Griggs, Theodor, additional, Sharma, Dhara, additional, Kaur, Prabhdeep, additional, Priyamavada, Shubha, additional, Jayawardena, Dulari, additional, Kumar, Anoop, additional, Saksena, Seema, additional, Alrefai, Waddah, additional, Tan, Xiao-Di, additional, Dudeja, Pradeep, additional, and Gill, Ravinder, additional

Published
2023
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17. Feeding mode influences dynamic gut microbiota signatures and affects susceptibility to anti-CD3 mAb-induced intestinal injury in neonatal mice

Author

Subramanian, Saravanan, primary, Geng, Hua, additional, Du, Chao, additional, Chou, Pauline M., additional, Bu, Heng-Fu, additional, Wang, Xiao, additional, Swaminathan, Suchitra, additional, Tan, Stephanie C., additional, Ridlon, Jason M., additional, De Plaen, Isabelle G., additional, and Tan, Xiao-Di, additional

Published
2022
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24. Probiotic preparation VSL#3 alters the distribution and phenotypes of dendritic cells within the intestinal mucosa in C57BL/10J mice

Author

Wang, Xiao, O'Gorman, Maurice R.G., Bu, Heng-Fu, Koti, Viola, Zuo, Xiu-Li, and Tan, Xiao-Di

Subjects
Probiotics -- Usage, Probiotics -- Health aspects, Immune response -- Research, Intestines -- Research, Dendritic cells -- Research, Food/cooking/nutrition
Abstract

Probiotic nutrients have shown promise in therapy for the treatment of gastrointestinal inflammation, infection, and atopic disease. Intestinal dendritic cells (DC) play a critical role in shaping the intestinal immune response. In this study, we tested the effect of a probiotic preparation (VSL#3) on DC distribution and phenotypes within the intestinal mucosa using a lineage depletion-based flow cytometric analysis. In naive C57BL/10J mice, intestinal mucosal DC were composed of plasmacytoid DC (pDC) and myeloid DC (mDC). The pDC were the dominant form in lamina propria and Peyer's patches, whereas mDC were the prevailing type in the mesenteric lymph nodes. Additional characterization of pDC and mDC with flow cytometry revealed that they expressed heterogeneous phenotypes in the intestinal mucosa. In mice gavaged with the probiotic VSL#3 for 7 d, the proportion of pDC within the lamina propria was >60% lower, whereas the pDC subset in the mesenteric lymph nodes was more than 200% greater than in sham-treated controls (P < 0.01). Within pDC, the proportion of functionally unique [CX3CR1.sup.+] DC was greater than in controls in both the lamina propria and the Peyer's patches (P < 0.01). In contrast to pDC, the mDC number was greater than in controls in all intestinal lymphoid tissue compartments in VSL#3-treated mice (P < 0.01). In conclusion, this study suggests that phenotypically and functionally distinct DC subsets are localized to specific lymphoid tissues within the intestinal mucosa and that the VSL#3 probiotic nutritional supplement alters the distribution of the DC subsets within the intestinal mucosa. These changes may be important in the alteration of mucosal immunity following probiotic VSL#3 therapy. J. Nutr. 139:1595-1602, 2009.

Published
2009

26. Cell death of intestinal epithelial cells in intestinal diseases

Author

Subramanian, Saravanan, Geng, Hua, and Tan, Xiao-Di

Subjects
Necrosis, Cell Death, Infant, Newborn, Humans, Apoptosis, Epithelial Cells, Intestinal Mucosa, digestive system, digestive system diseases, Article
Abstract

Gut injury continues to be the devastating and unpredictable critical illness associated with increased cell death of intestinal epithelial cells (IECs). The IECs, immune system and microbiome are the interrelated entities to maintain normal intestinal homeostasis and barrier integrity. In response to microbial invasion, IEC cell death occurs to maintain intestinal epithelium function and retain the continuous renewal and tissue homeostasis. But the imbalance of IEC cell death results in increased intestinal permeability and barrier dysfunction that leads to several acute and chronic intestinal diseases, such as intestinal ischemia/reperfusion (I/R), sepsis, inflammatory bowel diseases (IBD), necrotizing enterocolitis (NEC), etc. During the pathophysiological state, the excessive IEC apoptotic cell death leads to a chronic inflammatory condition, later switches to necroptotic cell death mechanism that induces more pathological features than apoptosis and may also induce other lytic cell death mechanisms like pyroptosis and ferroptosis to increase the pathogenesis of the intestinal diseases. But still, there remains gaps in the fundamental knowledge about the IEC cell death mechanisms in chronic intestinal diseases. Together, a deep understanding of the specific cell death mechanisms underlying chronic intestinal diseases, including sepsis, IBD, NEC, and intestinal I/R, is desperately needed to develop emerging novel promising therapeutic strategies. This review aims to show how the acute and critical illness in the gut are driven by IEC cell death mechanism, such as apoptosis, necrosis, necroptosis, pyroptosis, and ferroptosis.

Published
2020

30. Milk fat globule-EGF factor 8/lactadherin plays a crucial role in maintenance and repair of murine intestinal epithelium

Author

Bu, Heng-Fu, Zuo, Xiu-Li, Wang, Xiao, Ensslin, Michael A., Koti, Vjola, Hsueh, Wei, Raymond, Adam S., Shur, Barry D., and Tan, Xiao-Di

Subjects
Intestinal mucosa -- Health aspects, Intestinal mucosa -- Research, Proteins -- Usage, Proteins -- Health aspects, Proteins -- Research, Wound healing -- Health aspects
Abstract

Milk fat globule-EGF factor 8 (MFG-E8)/lactadherin participates in several cell surface-mediated regulatory events. Although its mRNA is present in the gut, the physiological roles of MFG-E8 in the intestinal mucosa have not been explored. Here we show that MFG-E8 was expressed in intestinal lamina propria macrophages from mice. Using a wound-healing assay, MFG-E8 was shown to promote the migration of intestinal epithelial cells through a PKC[epsilon]-dependent mechanism. MFG-E8 bound to phosphatidylserine and triggered reorientation of the actin cytoskeleton in intestinal epithelial cells at the wound edge. Depleting MFG-E8 in mice by administration of anti-MFG-E8 antibody or targeted deletion of the MFG-E8 gene resulted in a slowing of enterocyte migration along the crypt-villus axis and focal mucosal injury. Moreover, in septic mice, intestinal MFG-E8 expression was downregulated, which correlated with intestinal injury, interrupted enterocyte migration, and impaired restitution. Treatment with recombinant MFG-E8 restored enterocyte migration, whereas deletion of MFG-E8 impeded mucosal healing in mice with sepsis. These results suggest that a decrease in intestinal MFG-E8 impairs intestinal mucosal repair in sepsis. Together, our data indicate that MFG-E8 plays an important role in the maintenance of intestinal epithelial homeostasis and the promotion of mucosal healing and suggest that recombinant MFG-E8 may be beneficial for the treatment of bowel injuries., Introduction Intestinal mucosa is covered with an epithelial lining that turns over rapidly and continuously throughout life. Cell proliferation, differentiation, and migration are crucial events required for the maintenance of [...]

Published
2007

40. Molecular mechanisms underlying the regulation of the MFG-E8 gene promoter activity in physiological and inflammatory conditions

Author

Wang, Xiao, Bu, Heng-Fu, Liu, Shirley XL, De Plaen, Isabelle G., and Tan, Xiao-Di

Subjects
Inflammation, Lipopolysaccharides, Binding Sites, Proto-Oncogene Proteins c-jun, Sp1 Transcription Factor, Milk Proteins, Article, Mice, Gene Expression Regulation, Antigens, Surface, Macrophages, Peritoneal, Animals, Promoter Regions, Genetic, Cells, Cultured
Abstract

Milk fat globule-EGF factor 8 (MFG-E8) is expressed by macrophages and plays an important role in attenuating inflammation and maintaining tissue homeostasis. Previously, we and others found that lipopolysaccharide (LPS) inhibits MFG-E8 gene expression in macrophages. Here, we characterized the 5'-flanking region of the mouse MFG-E8 gene. To functionally analyze the upstream regulatory region of the MFG-E8 gene, a series of luciferase reporter gene constructs containing deleted or mutated regulatory elements were prepared. Using the luciferase assay, we revealed that Sp1 binding motifs within the proximal promoter region were necessary for full activity of the MFG-E8 promoter, whereas AP-1 like binding sequence at -372 played a role in governing the promoter activity at a homeostatic level. With chromatin immunoprecipitation assay, we showed that Sp1 and c-Jun physically interact with the MFG-E8 promoter region in vivo. In addition, Sp1 was found to regulate the MFG-E8 promoter activity positively and c-Jun negatively. Furthermore, we demonstrated that LPS inhibited MFG-E8 promoter activity via targeting Sp1 and AP-1-like motifs in the 5'-flanking region. Collectively, our data indicate that Sp1 and AP-1-related factors are involved in the regulation of MFG-E8 gene transcription by targeting their binding sites in the 5'-flanking region under physiological and inflammatory states.

Published
2015

45. Blocking NF-κB Activation in Ly6c+Monocytes Attenuates Necrotizing Enterocolitis

Author

Managlia, Elizabeth, Liu, Shirley X.L., Yan, Xiaocai, Tan, Xiao-Di, Chou, Pauline M., Barrett, Terrence A., and De Plaen, Isabelle G.

Abstract

Necrotizing enterocolitis (NEC) is a devastating disease affecting premature infants with intestinal inflammation and necrosis. The neonatal intestinal inflammatory response is rich in macrophages, and blood monocyte count is low in human NEC. We previously found that NF-κB mediates the intestinal injury in experimental NEC. However, the role of NF-κB in myeloid cells during NEC remains unclear. Herein, inhibitor of kappaB kinase β (IKKβ), a critical kinase mediating NF-κB activation, was deleted in lysozyme M (Lysm)–expressing cells, which were found to be Cd11b+Ly6c+monocytes but not Cd11b+Ly6c−macrophages in the dam-fed neonatal mouse intestine. NEC induced differentiation of monocytes into intestinal macrophages and up-regulation of monocyte recruitment genes (eg, L-selectin) in the macrophage compartment in wild-type mice, but not in pups with IKKβ deletion in Lysm+cells. Thus, NF-κB is required for NEC-induced monocyte activation, recruitment, and differentiation in neonatal intestines. Furthermore, pups with Lysm-IKKβ deletion had improved survival and decreased incidence of severe NEC compared with littermate controls. Decreased NEC severity was not associated with an improved intestinal barrier. In contrast, NEC was unabated in mice with IKKβ deletion in intestinal epithelial cells. Together, these data suggest that recruitment of Ly6c+monocytes into the intestine, NF-κB activation in these cells, and differentiation of Ly6c+monocytes into macrophages are critical cellular and molecular events in NEC development to promote disease.

Published
2019
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46. Su1847 H19 Is an Early Response Long Non-Coding RNA (lncRNA) Which Controls the Homeostasis of c-Fos Gene Expression in Intestinal Inflammation

Author

Geng, Hua, primary, Bu, Heng-Fu, additional, Pfeifer, Karl, additional, Wu, Longtao, additional, Pandey, Ashutosh K., additional, Liu, Fangyi, additional, Wang, Peng, additional, Wang, Xiao, additional, Akhtar, Suhail, additional, Lu, Lu, additional, Yu, Jindan, additional, and Tan, Xiao-Di, additional

Published
2015
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50. Milk fat globule-EGF factor 8 mRNA expression in rat splanchnic tissues during postnatal development

Author

Wang, Xiao, Bu, Heng-Fu, De Plaen, Isabelle G., and Tan, Xiao-Di

Subjects
Original Article
Abstract

Milk fat globule-EGF factor (MFG-E8) is a protein that binds to alphavbeta3/5 integrin and phosphatidylserine. It plays a role in apoptotic cell removal, tissue remodeling and intestinal epithelial wound-healing process. In the present study, we examined the expression of MFG-E8 mRNA in the small intestine, liver and lungs during postnatal development. Sprague-Dawley rats were sacrificed at different ages (E20, P0, P5, P10 and P21). Total RNA was extracted from various tissues including the small intestine, liver and lungs. The MFG-E8 mRNA expression was quantified by real-time PCR. We found that the MFG-E8 mRNA was expressed at a low level on E20 in the liver. Within 24 hours after birth, its expression was markedly increased. It was then stably expressed at high level during the postnatal period. In contrast, in the small intestine, MFG-E8 mRNA significantly decreased by more than 60% (p0.001) within 24 hours after birth compared to E20, then it gradually regained E20 values by P10. It was persistently expressed until P21. In the lungs, MFG-E8 is constitutively expressed prenatally at E20. Its expression did not change during the postnatal period. In summary, our study indicated that MFG-E8 is extensively expressed in the small intestine, liver, and lungs. As opposed to other organs, the expression of intestinal MFG-E8 is decreased during the first week of life. It is possible that this could contribute to the predisposition of the neonatal intestine to inflammation.

Published
2009

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