
Meenakshi Bewtra
VerifiedUniversity of Pennsylvania · Rehabilitation Medicine
Active 2002–2026
About
Meenakshi Bewtra, MD, PhD, MPH, is an Associate Professor of Medicine (Gastroenterology) at the Hospital of the University of Pennsylvania. She serves as an Attending Physician at Penn Medicine at Radnor, the Corporal Michael J. Crescenz Veteran's Affairs Medical Center, and the Hospital of the University of Pennsylvania. She is the Co-Section Head and Research and Education Director for Inflammatory Bowel Disease within the Division of Gastroenterology and Hepatology at the University of Pennsylvania. Her clinical expertise includes inflammatory bowel disease, ulcerative colitis, Crohn's disease, immune-mediated colitis, and microscopic colitis. Her research focuses on epidemiology, real-world data, discrete choice experiments, and clinical trials related to inflammatory bowel disease. She is actively involved in research initiatives such as the Inflammatory Bowel Disease Program at Penn Medicine and the IBD-Immunology Initiative (I3), which enrolls all IBD patients at UPenn and collaborates nationally and internationally. Dr. Bewtra's educational background includes a BSc from Yale University, an MD from the University of Pennsylvania, an MPH from Harvard University School of Public Health, and a PhD in Epidemiology from the University of Pennsylvania.
Research topics
- Internal medicine
- Medicine
- Gastroenterology
- Family medicine
- Biochemistry
- Surgery
- Chemistry
Selected publications
Gastrointestinal Endoscopy · 2026-05-01
articleDigestive Diseases and Sciences · 2026-03-09 · 1 citations
articleOpen accessBACKGROUND: Crohn's disease is a heterogeneous, transmural inflammatory condition that can involve any segment of the gastrointestinal tract. Distinct locations (ileal, colonic, ileocolonic) and phenotypes (inflammatory, stricturing, penetrating) display different clinical behaviors and complication risks in CD. Whether these location- and phenotype-specific patterns correspond to unique metabolomic profiles remains incompletely defined. METHODS: To identify metabolites associated with disease activity, location, and phenotype, ultrahigh performance liquid chromatography-tandem mass spectroscopy-based metabolomic analysis was performed on stool samples from patients with CD. Active CD was defined as patients with fecal calprotectin above 100 μg/g. Metabolite differences among groups were assessed using permutational multivariate analysis of variance. Candidate metabolites were identified and validated using multivariable linear models adjusting for demographic covariates, with false discovery rate correction. RESULTS: A total of 302 stool samples from patients with CD were analyzed. Complicated CD phenotypes (B2 and B3) showed increased acylcarnitines and secondary bile acids compared with inflammatory (B1) phenotype. Location-specific analysis indicated increased cholate, and N-acyl ethanolamides in ileal and ileocolonic compared to colonic CD. When stratified by inflammation using fecal calprotectin, patients with active disease displayed upregulation of methylysine, ceramide, sphingomyelin, and polyamines. CONCLUSION: This study reveals metabolomic differences across CD phenotypes and disease activity, providing potential noninvasive biomarkers to help risk-stratify patients for complications and guide tailored management. Further validation in larger cohorts is warranted.
Gastroenterology · 2026-05-01
articleGastroenterology · 2026-05-01
articleArthritis Care & Research · 2026-04-20
articleOpen accessOBJECTIVE: The concern that nonsteroidal anti-inflammatory drugs (NSAIDs) may precipitate flares of inflammatory bowel disease (IBD) has limited their use in managing musculoskeletal symptoms in those with IBD, but safety data are mixed. METHODS: This retrospective cohort study included patients with IBD aged at least 18 years from Optum's deidentified Clinformatics Data Mart Database (2000-2022). Patients with a new NSAID prescription fill were matched to those without an NSAID fill during the study period. The index date for exposed patients was the date of first NSAID fill, with a matched date for unexposed. Propensity score-based inverse probability of treatment-weighted Cox proportional hazards models evaluated the association between NSAID exposure and time to IBD-related hospitalization across IBD subtypes. A hazard ratio (HR) of 1.2 was prespecified as the non-inferiority margin. RESULTS: Among 348,095 patients with IBD, 23.2% were NSAID-exposed. NSAID exposure was associated with a small increase in IBD-related hospitalization in the overall cohort but demonstrated non-inferiority (HR 1.07, 95% confidence interval [CI] 1.04-1.10). Non-inferiority was met with no significantly increased risk of IBD-related hospitalization in patients with ulcerative colitis (HR 0.97, 95% CI 0.93-1.02). In contrast, non-inferiority was not met in the Crohn disease subgroup (HR 1.16, 95% CI 1.12-1.21). CONCLUSION: Patients with ulcerative colitis did not have a significantly increased risk of IBD-related hospitalization associated with NSAID exposure and met non-inferiority, whereas non-inferiority could not be established for those with Crohn disease. These results suggest that NSAID use may be acceptable for select patients with IBD who have significant musculoskeletal symptoms, especially those with ulcerative colitis.
Gastrointestinal Endoscopy · 2026-05-01
articleGastrointestinal Endoscopy · 2026-05-01
articleGastroenterology · 2026-05-01
articleAn Epigenetic Basis for Sustained Inflammatory Epithelial Progenitor Cell States in Crohn’s Disease
Cellular and Molecular Gastroenterology and Hepatology · 2025-10-21 · 1 citations
articleOpen accessBACKGROUND & AIMS: Defining consequential differences in intestinal epithelial stem cells in healthy humans vs those with inflammatory bowel disease (Crohn's disease and ulcerative colitis) is essential for the development of much needed therapies to restore the epithelial barrier and maintain its fidelity. METHODS: We used single-cell transcriptomic and epigenomic approaches in matched patient tissues and organoids to investigate epithelial gene expression and function in children with no pathological diagnosis in the lower gastrointestinal tract and healthy adults compared with those with Crohn's disease. RESULTS: We identify an inflammatory secretory progenitor (ISP) cell state present almost exclusively in patients with Crohn's disease compared with healthy subjects. ISPs exhibit gene expression profiles consistent with normal secretory progenitor cells but concomitantly express a suite of distinguishing pro-inflammatory genes. Mechanistically, ISPs exhibit open chromatin at ISP gene loci. Although ISP-specific genes are not expressed in intestinal stem cells, their chromatin is accessible in Crohn's disease stem cells, suggesting that ISP genes are epigenetically poised in stem cells and subsequently transcriptionally activated in ISPs in the presence of inflammatory stimuli. Consistently, Crohn's disease colonoids exhibit sustained ISP gene expression that can be elicited further with pro-inflammatory cytokines or via co-culture with pro-inflammatory macrophages. CONCLUSIONS: We have defined differences in the epithelial stem and progenitor compartment of patients with Crohn's disease that suggest aberrant stem cell differentiation and inflammatory gene expression arise and persist during disease.
Journal of Crohn s and Colitis · 2025-01-01
articleOpen accessAbstract Background Comprising about 40% of mucosal lymphocytes, γδ T cells represent a significant lineage in the gut, and thus are key players in the intestinal immune homeostasis. In contrast to αβ TCRs, γδ TCRs are able to recognize antigen independent from MHC-restricted antigen presentation. While antigens recognized by γδ TCRs are largely undefined, activation of γδ T cells is initiated by phospho-antigens and members of the butyrophilin (BTN) family. Data from both murine and human studies suggest a protective role of γδ T cells in the pathogenesis of inflammatory bowel diseases (IBD). However, significant species-specific variations of γδ T cells demand more detailed investigation of human intestinal γδ T cells. To date, no single-cell study has comprehensively assessed subset-related roles of γδ T cells in ulcerative colitis (UC). Methods In this study, we performed multimodal profiling of intestinal γδ T cells in ulcerative colitis (UC) at single-cell resolution using FLASH-seq (healthy donors (HD) n=2, active UC n=5) and cytometry by time of flight (CyTOF, HD n=29, inactive UC n=26, active UC n=24). FLASH-seq analysis of additional samples is ongoing. Peripheral blood samples were analyzed in a subset of patients. Results Our analysis revealed that healthy gut epithelium is predominantly populated by CD103+ intraepithelial γδ lymphocytes (γδ IELs). However, in the inflamed intestinal environment, two distinct although clonally related γδ T cell subsets emerge: one TCF-1+ PD-1+ memory-like subset, resembling stem-like αβ T cells previously described in chronic infections and cancer, and the other exhibiting a cytotoxic phenotype, characterized by increased expression of GZMB, PRF1, and TBX21. The decline in CD103+ γδ T cells, coupled with the expansion of these two subsets, was associated with reduced expression of butyrophilin-like (BTNL) molecules, BTNL3 and BTNL8, and increased expression of BTN3A1 and BTN3A3, along with transcriptional and metabolic changes associated with enhanced γδ T cell-mediated killing in intestinal epithelial cells. Patients responding to therapies showed a return to a healthy γδ T cell subset composition, with the contraction of these subsets after remission, further supporting their pathogenic role. Additionally, significant opposing phenotypic changes were observed in peripheral blood γδ T cell subsets in UC. Conclusion Overall, our data provide a comprehensive single-cell landscape of γδ T cells in UC, identifying novel subsets that differentially carry out protective and pathogenic roles. These subsets may serve as valuable biomarkers, and may represent novel therapeutic targets.
Recent grants
NIH · $763k · 2014
Frequent coauthors
- 1034 shared
Sumona Saha
UW Health University Hospital
- 1028 shared
David Hudesman
- 524 shared
Raymond K. Cross
University of Maryland, Baltimore
- 523 shared
Scott B. Snapper
Harvard University
- 518 shared
David L. Suskind
Seattle Children's Hospital
- 517 shared
Themistocles Dassopoulos
Wockhardt (United States)
- 517 shared
Freddy Caldera
Pfizer (United States)
- 516 shared
Shrinivas Bishu
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