Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Our purpose was to determine if cytokines are produced systemically during acute pancreatitis. Proinflammatory cytokines are elevated during acute pancreatitis and have been implicated in the progression of pancreatitis-associated multiple organ dysfunction. Whether these mediators are produced within all tissues or very few specific organs is not known. Edematous pancreatitis was induced in adult male mice by IP injection of cerulein. Necrotizing pancreatitis was induced in young female mice by feeding a choline-deficient, ethionine supplemented diet. Animals were sacrificed as pancreatitis worsened, with multiple organs prepared for tissue mRNA and protein analysis by RT-PCR and immunoblotting. Pancreatitis severity was established by histologic grading and serum amylase and lipase. There was no cytokine mRNA or protein detectable prior to the induction of pancreatitis. Tumor necrosis factor-alpha (TNF-alpha) and interleukin-1-beta (IL-1 beta) mRNA and protein were detected within the pancreas early in the course of pancreatitis in both models, coinciding with the development of hyperamylasemia (both P < 0.001). Interleukin-6 was produced in the pancreas after pancreatitis was more fully developed (P < 0.001). IL-1 beta and TNF-alpha were subsequently produced in large amounts in lung, liver, and spleen but never within kidney, cardiac muscle, or skeletal muscle. A significant delay between pancreatic and distant organ cytokine production was always observed. It is concluded that proinflammatory cytokines are produced within the pancreas and within organs known to develop dysfunction during severe pancreatitis. Cytokine production is tissue specific, correlates with disease severity, and occurs within the pancreas first and subsequently within distant organs.
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PMID:Tissue-specific cytokine production during experimental acute pancreatitis. A probable mechanism for distant organ dysfunction. 928 48

Six piglets aged 20 days were inoculated oranasally with 5 ml of a suspension (10(6) TCID(50)/ml) of a Greek myocardial strain of encephalomyocarditis virus (EMCV). The animals either died (n=2) or were killed for examination on days 1,2 or 3 post-inoculation (pi). EMCV was isolated from virtually all organs examined (heart, tonsils, palatine glands, pancreas, spleen, small intestine and mesenteric lymph nodes). Histopathologically, interstitial myocarditis, necrosis of cardiac muscle cells and Purkinje fibres, and necrotizing tonsillitis were detected in all inoculated piglets. Focal interstitial pancreatitis, necrosis of pancreatic acinar cells and Langerhans islet cells, and necrosis of germinal centre lymphocytes of the lymph nodes and Peyer's patches were detected in two piglets that died or were killed on day 3 pi. Immunohistochemically, viral antigen was detected in epithelial cells of all organs examined, including the tonsils, palatine glands, pancreatic interlobular ducts and small intestine. This suggests that EMCV is epitheliotropic, in addition to its known myocardial tropism. The frequent presence of intracytoplasmic EMCV in macrophages of the tonsils and spleen supports the hypothesis that macrophages play a role in viral replication and dissemination in the body.
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PMID:Pathogenesis of encephalomyocarditis virus (EMCV) infection in piglets during the viraemia phase: a histopathological, immunohistochemical and virological study. 1292 22

Rats (n=40) aged 8 weeks were infected, either by oronasal inoculation or by contact, with one of two different myocardial strains of encephalomyocarditis virus (EMCV), namely, the Greek strain 424/90 and the Belgian strain B279/95. The animals were killed at 11-62 days post-infection (dpi) and samples of brain, heart, pancreas, kidney, Peyer's patches, spleen, lung and thymus were processed for virological, histopathological and immunohistochemical evaluation. This experimental infection was inapparent, but virus was isolated from faeces and several organs of all animals. The main histopathological changes were focal interstitial pancreatitis, degeneration and necrosis of pancreatic acinar cells, depletion of thymus and Peyer's patches, and interstitial pneumonia. EMCV antigen was detected in the cytoplasm of cardiac muscle cells, pancreatic acinar cells and hepatic epithelial cells, and in macrophages of the spleen, lung and thymus. In the heart (the target organ of EMCV in pigs), the presence of EMCV in cardiac muscle cells without lesions lends support to the hypothesis that the rat is a natural reservoir host species of EMCV. The persistence of virus in the macrophages of the thymus may represent a mechanism of perpetuation and reactivation, under immunosuppressive conditions, of the infection.
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PMID:Pathogenesis of experimental encephalomyocarditis: a histopathological, immunohistochemical and virological study in rats. 1633 40

Mice (n=20) aged 8 weeks were infected, either by oronasal inoculation or by contact, with one of two different myocardial strains of encephalomyocarditis virus (EMCV), namely, the Greek strain 424/90 and the Belgian strain B279/95. The animals were killed at 18-59 days post-infection (dpi), except for two mice that died at 6 and 32 dpi, and samples of brain, heart, pancreas, kidney, Peyer's patches, spleen, lung and thymus were processed for virological, histopathological and immunohistochemical examination. Apart from the two deaths, the experimental infection was inapparent, but virus was invariably recovered from faeces and several organs. The main histopathological lesions were focal interstitial pancreatitis, depletion of thymus and Peyer's patches, and interstitial pneumonia. Additionally, in the two mice that died, multifocal interstitial myocarditis was observed. EMCV antigen was detected in the cytoplasm of pancreatic acinar cells and in macrophages of the lung and the thymus. Antigen was also detected in the cytoplasm of cardiac muscle cells from three animals, including the two that died. The results support the role of mice, in addition to rats, as reservoir hosts in the epidemiology of EMCV infections on pig farms.
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PMID:Pathogenesis of experimental encephalomyocarditis: a histopathological, immunohistochemical and virological study in mice. 1695 70

Fibroblast growth factor 21 (FGF21) is a peptide hormone that is synthesized by several organs and regulates energy homeostasis. Excitement surrounding this relatively recently identified hormone is based on the documented metabolic beneficial effects of FGF21, which include weight loss and improved glycemia. The biology of FGF21 is intrinsically complicated owing to its diverse metabolic functions in multiple target organs and its ability to act as an autocrine, paracrine, and endocrine factor. In the liver, FGF21 plays an important role in the regulation of fatty acid oxidation both in the fasted state and in mice consuming a high-fat, low-carbohydrate ketogenic diet. FGF21 also regulates fatty acid metabolism in mice consuming a diet that promotes hepatic lipotoxicity. In white adipose tissue (WAT), FGF21 regulates aspects of glucose metabolism, and in susceptible WAT depots, it can cause browning. This peptide is highly expressed in the pancreas, where it appears to play an anti-inflammatory role in experimental pancreatitis. It also has an anti-inflammatory role in cardiac muscle. Although typically not expressed in skeletal muscle, FGF21 is induced in situations of muscle stress, particularly mitochondrial myopathies. FGF21 has been proposed as a novel therapeutic for metabolic complications such as diabetes and fatty liver disease. This review aims to interpret and delineate the ever-expanding complexity of FGF21 physiology.
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PMID:Understanding the Physiology of FGF21. 2665 52