ArticlePloS one2015
Somatostatin Improved B Cells Mature in Macaques during Intestinal Ischemia-Reperfusion.
Article in PloS one, 2015. 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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Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- Prevention of Severe Acute Pancreatitis With Cyclooxygenase-2 Inhibitors: A Randomized Controlled Clinical Trial.The American journal of gastroenterology · 2020Trial
- Somatostatin and Its Analogues as Second-Line Treatments in Non-Neoplastic Conditions.International journal of molecular sciences · 2026Review
- The Role of Somatostatin in the Gastrointestinal Tract.Biology · 2025Review
- Germacrone ameliorates acute lung injury induced by intestinal ischemia-reperfusion by regulating macrophage M1 polarization and mitochondrial defects.Acta biochimica et biophysica Sinica · 2024Article
- Plasma Somatostatin Levels Increase during Scoliosis Surgery, but Not Herniated Disc Operations: Results of a Pilot Study.Biomedicines · 2023Article
- Commensal microbiota modulates phenotypic characteristics and gene expression in piglet Peyer's patches.Frontiers in physiology · 2023Article
- Identification of two downregulated circRNAs in patients with acute B-lymphocytic leukemia.Oncology letters · 2022Article
- Aggravated intestinal ischemia‑reperfusion injury is associated with activated mitochondrial autophagy in a mouse model of diabetes.Molecular medicine reports · 2020Article
- Protective Role of Somatostatin in Sepsis-Induced Intestinal Barrier Dysfunction through Inhibiting the Activation of NF-Gastroenterology research and practice · 2020Article
- Enteroendocrine cells-sensory sentinels of the intestinal environment and orchestrators of mucosal immunity.Mucosal immunology · 2018Review
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Authors and funding
7 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
aimsIntestinal ischemia-reperfusion has been taken as an important pathophysiological process for multiple organ dysfunctions in critical patients. Recent studies reported that dual expression programs of the B cells receptors and Toll-like receptors on B-lymphocytes permit these ubiquitous cells to integrate both adaptive and innate immune functions. Our previous studies found that somatostatin inhibited the intestinal inflammatory injury after ischemia-reperfusion in macaques. However, the changes of B cells and the effects of somatostatin on B cells after intestinal ischemia-reperfusion were unclear.
methods15 macaques were divided into control, intestinal ischemia-reperfusion and somatostatin pretreatment groups. Immunohistochemistry was performed to identify the distributions of adaptive and innate immunity markers in the iliac mucosa. Hmy2.cir B lymphoblastoid cell line was cultured in vitro study. Enzyme-linked immunosorbent assay was used to measure IgM, IL-6 and SIgA, and the expressions of B cells transcription factors, PAX-5 and BLIMP-1, were detected by Western blotting.
resultsB2 lymphocytes in normal Peyer's patches were presented the phenotype of PAX-5+CD20+CD5-. Ischemia-reperfusion increased the numbers and sizes of Peyer's patches but with PAX-5+CD20-CD5- B cells, an unmatured set of B cells. Somatostatin partly kept the phenotype of mature B cells during ischemia-reperfusion. The innate immunity of B cells was inhibited whereas the adaptive immunity was increased in the intestinal mucosa in the somatostatin group, compared to the ischemia-reperfusion group. In vitro, somatostatin significantly inhibited IL-6 and promoted IgM by increasing the expression of both PAX-5 and BLIMP-1 in the proinflammatory condition.
conclusionIntestinal ischemia-reperfusion resulted in the proliferation of unmatured B cells which were involved in the augmentation of innate immunity. Somatostatin, with a bi-directional regulation function on innate as well as adaptive immunity of B cells, greatly improved B cells mature in macaques during ischemia-reperfusion. Preventive supplements of somatostatin may greatly limit intestinal injury and bacterial translocation during ischemia-reperfusion.
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