ReviewInternational journal of colorectal disease2014
Experimental appendicitis and appendectomy modulate the CCL20-CCR6 axis to limit inflammatory colitis pathology.
Review in International journal of colorectal disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
10 citing papers in PubMed, 19 citations in OpenAlex.
- Distinct microbiota composition and dendritic cell activation in the appendix microenvironment of ulcerative colitis patients.Gut microbes · 2025Article
- Identification of the Binding Epitope of an Anti-Mouse CCR6 Monoclonal Antibody (CAntibodies (Basel, Switzerland) · 2023Article
- Interleukin-26 Expression in Inflammatory Bowel Disease and Its Immunoregulatory Effects on Macrophages.Frontiers in medicine · 2022Article
- Molecular pathogenesis involved in human idiopathic pulmonary fibrosis based on an integrated microRNA‑mRNA interaction network.Molecular medicine reports · 2018Article
- The Role of Specific Chemokines in the Amelioration of Colitis by Appendicitis and Appendectomy.Biomolecules · 2018Article
- Expression of CCR6 in esophageal squamous cell carcinoma and its effects on epithelial-to-mesenchymal transition.Oncotarget · 2017Article
- Identification of intraocular inflammatory mediators in patients with endophthalmitis.Molecular vision · 2016Article
- The research conundrum of acute appendicitis.The British journal of surgery · 2015Review
- Inflammatory bowel disease: Traditional knowledge holds the seeds for the future.World journal of gastrointestinal pharmacology and therapeutics · 2015Article
- Inflammatory bowel disease pathobiology: the role of the interferon signature.Annals of gastroenterologyReview
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCrohn's disease and ulcerative colitis are the two spectral variations of inflammatory bowel diseases (IBD). The complex interplay between genetic predisposition, gastrointestinal bacteria, and gut immunity in IBD is yet to be deciphered. The newly described IL-17-secreting subset of CD4+ T cells, called Th17 cells (and its "Th17 system"), has been increasingly implicated in the pathogenesis of inflammatory changes in inflammatory/autoimmune diseases including IBD. The chemokine ligand CCL20 and its receptor CCR6 are both upregulated in colon biopsy samples during active IBD. Appendicitis and appendectomy (AA) prevents or significantly ameliorates human IBD.
methodsWe pioneered the first animal model of AA. AA was performed on 5-week-old male BALB/c mice, and distal-colon samples were harvested. Mice with two laparotomies each served as sham and sham (SS) controls. RNA was extracted from individual colonic replicate samples (AA and SS groups) and each sample microarray analyzed and reverse transcription-polymerase chain reaction (RT-PCR) validated. Gene set enrichment analysis (GSEA) software was used to further analyze the microarray data.
resultsPrior AA ameliorates experimental colitis in our murine model. CCL20 expression was significantly suppressed (along with components of the Th17 system) in the most distal colon 3 and 28 days after AA was done at the most proximal colon.
conclusionTeasing out the pathways involved in the changes induced by AA on the colon in clinical studies and, most importantly, in our unique murine AA model will lead to the development of techniques to manipulate different components of the CCL20-CCR6 axis and Th17 system resulting in significant advances in IBD management.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.