Crohn's disease is a chronic inflammatory disorder primarily affecting the gastrointestinal tract. Its clinical manifestations arise from a substantial infiltration of the intestinal mucosa by activated leukocytes and the downstream consequences of chronic inflammation. The underlying cause driving this immunological reaction remains poorly understood. A number of hypotheses have been proposed, most of which postulate a primary over-activation of the immune response, based on the pathological appearances of active Crohn's lesions. Interestingly, none of these theories have been mechanistically proven. It is possible that the immunological events responsible for disease initiation are quite different from those contributing to its persistence and propagation. A substantial body of data has emerged in recent years to suggest that the primary defect in Crohn's disease is actually one of relative immunodeficiency. This review considers the evidence for such a phenomenon in contrast to alternative prevailing hypotheses and attempts to address some of the potential paradoxes that it generates.
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http://dx.doi.org/10.1007/s12016-009-8133-2 | DOI Listing |
ACS Biomater Sci Eng
January 2025
Department of Gastrointestinal Surgery, Affiliated Hospital of Nantong University, Medical School of Nantong University, Nantong 226001, China.
Perianal fistulas (PAFs) are a severe complication of Crohn's disease that significantly impact patient prognosis and quality of life. While stem-cell-based strategies have been widely applied for PAF treatment, their efficacy remains limited. Our study introduces an injectable, temperature-controlled decellularized adipose tissue-alginate hydrogel loaded with dental pulp mesenchymal stem cells (DPMSCs) for in vivo fistula treatment.
View Article and Find Full Text PDFJ Crohns Colitis
January 2025
Division of Clinical Epidemiology, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden.
Background And Aims: Nationwide, population-based studies of chronic non-bacterial osteomyelitis (CNO) in patients with childhood-onset inflammatory bowel disease (IBD) are lacking.
Methods: We used nationwide registers to identify all children in Sweden diagnosed with IBD during 2002-2022 and the occurrence of CNO in this IBD cohort and general population non-IBD comparators. To estimate the temporal associations between IBD and CNO we used Cox regression.
J Crohns Colitis
January 2025
Department of Medicine (Division of Gastroenterology) and Farncombe Family Digestive Health Research Institute; McMaster University, Hamilton ON, Canada.
Introduction: In inflammatory bowel disease (IBD), the number of eosinophils increases in the lamina propria of the intestinal tract, but their specific patho-mechanistic role remains unclear. Elevated blood eosinophil counts in active IBD suggest their potential as biomarkers for predicting response to biologic therapies. This study evaluates blood eosinophil count trends and their predictive value for clinical response and endoscopic improvement in patients with IBD receiving ustekinumab or adalimumab induction therapy.
View Article and Find Full Text PDFEgypt J Immunol
January 2025
Department of Biology, Faculty of Science, University of Kufa, Najaf, Iraq.
Inflammatory bowel disease (IBD) is a protracted, persistent gastrointestinal disease that is distinguished by recurring, persistent inflammation of the digestive tract. IBD, including Crohn's disease and ulcerative colitis, is characterized by persistent inflammation due to immune dysregulation. Interleukin -17 (IL-17) contributes significantly to the pathophysiology of IBD, as highlighted in the context of the provided research.
View Article and Find Full Text PDFThe structure and function of the mammalian gut vary by region, yet why inflammatory diseases manifest in specific regions and not others remains unclear. We use a TNF-overexpressing Crohn's disease (CD) model (Tnf ), which typically presents in the terminal ileum (TI), to investigate how environmental factors interact with the host's immune susceptibility to drive region-specific disease. We identified , an intracellular bacterium and murine counterpart to the human sexually transmitted , as necessary and sufficient to trigger disease manifestation in the ascending colon (AC), another common site of human CD.
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