Increased Chromogranin A–Positive Hormone-Negative Cells in Chronic Pancreatitis
| Autor: | Peter C. Butler, Sangeeta Dhawan, Abu Saleh Md Moin, Sarah M. Dry, Allison Ong, Megan Cory, Jennifer M. Choi, Alexandra E. Butler, Robert A. Rizza |
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| Rok vydání: | 2018 |
| Předmět: |
Male
0301 basic medicine medicine.medical_specialty Chemokine Receptors CXCR3 Endocrinology Diabetes and Metabolism Clinical Biochemistry 030209 endocrinology & metabolism Inflammation Enteroendocrine cell Biochemistry Neogenesis Islets of Langerhans 03 medical and health sciences 0302 clinical medicine Endocrinology Pancreatitis Chronic Internal medicine medicine Humans CXCL10 Pancreas Clinical Research Articles Aged biology Chemistry Biochemistry (medical) Chromogranin A Middle Aged biology.organism_classification Chemokine CXCL10 030104 developmental biology medicine.anatomical_structure biology.protein Female medicine.symptom Hormone |
| Zdroj: | The Journal of Clinical Endocrinology & Metabolism. 103:2126-2135 |
| ISSN: | 1945-7197 0021-972X |
| DOI: | 10.1210/jc.2017-01562 |
| Popis: | Context Chronic pancreatitis (CP) is characterized by inflammation, fibrosis, and a loss of pancreatic acinar cells, which can result in exocrine and eventually endocrine deficiency. Pancreatitis has been reported to induce formation of new endocrine cells (neogenesis) in mice. Our recent data have implicated chromogranin A–positive hormone-negative (CPHN) cells as potential evidence of neogenesis in humans. Objective We sought to establish if CPHN cells were more abundant in CP in humans. Design, Setting, and Participants We investigated the frequency and distribution of CPHN cells and the expression of the chemokine C-X-C motif ligand 10 (CXCL10) and its receptor chemokine C-X-C motif receptor 3 in pancreas of nondiabetic subjects with CP. Results CPHN cell frequency in islets was increased sevenfold in CP [2.1% ± 0.67% vs 0.35% ± 0.09% CPHN cells in islets, CP vs nonpancreatitis (NP), P < 0.01], as were the CPHN cells found as scattered cells in the exocrine areas (17.4 ± 2.9 vs 4.2 ± 0.6, CP vs NP, P < 0.001). Polyhormonal endocrine cells were also increased in CP (2.7 ± 1.2 vs 0.1 ± 0.04, CP vs NP, % of polyhormonal cells of total endocrine cells, P < 0.01), as was expression of CXCL10 in α and β cells. Conclusion There is increased islet endogenous expression of the inflammation marker CXCL10 in islets in the setting of nondiabetic CP and an increase in polyhormonal (insulin-glucagon expressing) cells. The increase in CPHN cells in CP, often in a lobular distribution, may indicate foci of attempted endocrine cell regeneration. |
| Databáze: | OpenAIRE |
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