Jyotsna Chandra

ORCID: 0000-0003-0689-8918
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Research Areas
  • Inflammatory Bowel Disease
  • Pancreatitis Pathology and Treatment
  • Microscopic Colitis
  • Pancreatic and Hepatic Oncology Research
  • Helicobacter pylori-related gastroenterology studies
  • Digestive system and related health
  • Eosinophilic Esophagitis
  • Autoimmune and Inflammatory Disorders
  • Lipid metabolism and disorders
  • Gut microbiota and health
  • IL-33, ST2, and ILC Pathways
  • Phagocytosis and Immune Regulation
  • Hernia repair and management
  • Single-cell and spatial transcriptomics
  • Surgical Simulation and Training
  • Phenothiazines and Benzothiazines Synthesis and Activities
  • Acupuncture Treatment Research Studies
  • Therapeutic Uses of Natural Elements
  • Escherichia coli research studies
  • Alkaline Phosphatase Research Studies
  • Antimicrobial Peptides and Activities
  • Sphingolipid Metabolism and Signaling
  • Gastrointestinal motility and disorders
  • Galectins and Cancer Biology
  • Fibroblast Growth Factor Research

Cleveland Clinic
2019-2024

Cleveland Clinic Lerner College of Medicine
2022-2024

Calcutta National Medical College and Hospital
1962

Objective Creeping fat, the wrapping of mesenteric fat around bowel wall, is a typical feature Crohn’s disease, and associated with stricture formation obstruction. How creeping forms unknown, we interrogated potential mechanisms using novel intestinal tissue cell interaction systems. Design Tissues from normal, UC, non-strictured strictured disease specimens were obtained. The muscularis propria matrisome was determined via proteomics. Mesenteric explants, primary human preadipocytes...

10.1136/gutjnl-2020-323719 article EN Gut 2021-01-19

Objective Intestinal fibrosis is considered an inevitable consequence of chronic IBD, leading to stricture formation and need for surgery. During the process fibrogenesis, extracellular matrix (ECM) components critically regulate function mesenchymal cells. We characterised composition ECM in fibrostenosing Crohn’s disease (CD) control tissues. Design Decellularised full-thickness intestinal tissue platforms were tested using three different protocols, phenotypes was explored by proteomics...

10.1136/gutjnl-2022-328608 article EN Gut 2024-02-20

Introduction Intestinal fibrosis is a common and serious complication of inflammatory bowel diseases (IBD) driving stricture formation in Crohn's disease patients leading to submucosal damage ulcerative colitis. Recent studies provided novel insights into the role immune nonimmune components pathogenesis intestinal fibrosis. Those new findings may accelerate development anti-fibrotic treatment IBD patients.

10.1080/1744666x.2024.2330604 article EN Expert Review of Clinical Immunology 2024-03-13

Journal Article Further observations on cholera enterotoxin Get access S.N. De, De Department of Pathology, Medical College, Calcutta, India Search for other works by this author on: Oxford Academic PubMed Google Scholar M.L. Ghose, Ghose J. Chandra Transactions The Royal Society Tropical Medicine and Hygiene, Volume 56, Issue 3, May 1962, Pages 241–245, https://doi.org/10.1016/0035-9203(62)90161-X Published: 01 1962

10.1016/0035-9203(62)90161-x article EN Transactions of the Royal Society of Tropical Medicine and Hygiene 1962-05-01

Abstract Background Intestinal fibrosis is a significant clinical problem in Inflammatory bowel disease (IBD). This may lead to intestinal strictures induced by excessive accumulation of extracellular matrix (ECM) produced human myofibroblasts (HIMF). Transglutaminase (TG)2 covalently cross-links ECM-associated proteins, increases ECM stiffness and has direct pro-fibrotic effects. We investigated the role TG2 tissues, HIMF transgenic mouse models. Methods was detected tissues from Crohn’s...

10.1093/ecco-jcc/jjad212.0247 article EN Journal of Crohn s and Colitis 2024-01-01

Abstract Background S1P receptor (S1PR)1/5 modulators have been tested successfully in clinical development programs ulcerative colitis (UC), leading to their FDA approval. They are believed act through lymphocyte redistribution peripheral lymphoid tissue and reduced numbers of circulating lymphocytes, but evidence from other organs suggests potential additional mechanisms action. Methods A post-hoc analysis the phase 3 trial S1PR1/5 modulator Ozanimod patients with moderately severely...

10.1093/ecco-jcc/jjad212.0022 article EN Journal of Crohn s and Colitis 2024-01-01

Fibroblasts play a key role in stricture formation Crohn's disease (CD) but understanding it's pathogenesis requires systems-level investigation to uncover new treatment targets. We studied full thickness CD tissues characterize fibroblast heterogeneity and function by generating the first single cell RNA sequencing (scRNAseq) atlas of strictured bowel providing proof principle for therapeutic target validation.

10.1101/2023.04.03.534781 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2023-04-04

Abstract Background Mesenteric fat wrapping around the intestinal wall, so called ‘creeping fat’ (CF), is spatially linked with stricture formation in Crohn’s disease (CD). Intestinal muscularis propria (MP) smooth muscle cell (HIMC) hyperplasia a major contributor to luminal narrowing stricturing CD. We investigated CF derived factors and their effect on HIMC vitro vivo using human tissues, primary cells colitis model. Methods Secretion of free fatty acids (FFA) by mesenteric (MF) or organ...

10.1093/ecco-jcc/jjac190.0223 article EN Journal of Crohn s and Colitis 2023-01-30

Abstract Background Intestinal fibrosis is considered an inevitable consequence of chronic inflammatory bowel disease (IBD), leading to stricture formation and need for surgery. During the process fibrogenesis, extracellular matrix (ECM) components critically regulate function mesenchymal cells. We characterized composition ECM in fibrostenosing Crohn’s (CD) control tissues. Methods Decellularized full thickness intestinal tissue platforms were tested using three different protocols...

10.1093/ecco-jcc/jjac190.0072 article EN Journal of Crohn s and Colitis 2023-01-30
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