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)

The role of natural killer (NK) cells in the early immune response to a pancreatropic isolate of coxsackievirus B4 (CVB4) was investigated in a murine model of pancreatitis. Endogenous (background) NK cell activity in fresh spleen effector cells from eight mouse strains was compared with virus-augmented NK cell activity 4 days post-infection (p.i.). A significant virus-induced increase (P less than or equal to 0.003) in NK cell activity was seen in seven of eight infected mouse strains, when virus titres in the pancreas were beginning to fall. Lesions in the exocrine pancreas were least extensive in the three strains with the highest endogenous NK cell activity. In C3H/HeJ mice that had been depleted of NK cells prior to infection with a low virus concentration, resistance to infection of the pancreas was completely abolished; myocarditis was also observed in one of these animals. Thus, NK cells may limit virus replication in the pancreas and play a role in resistance in C3H/HeJ mice. Virus-specific neutralizing antibody was not detected in the serum until 5 to 6 days p.i. in most strains and did not appear to influence pancreatic virus titres. It may be significant that CVB4 infection did not induce the expression of major histocompatibility complex (MHC) class I molecules on target acinar cells. With certain tumour cells, an inverse relationship between MHC class I expression and susceptibility to NK cell-mediated lysis is well documented.
 ...
PMID:Coxsackievirus B4 infection of the mouse pancreas: the role of natural killer cells in the control of virus replication and resistance to infection. 160 59

A chimeric virus containing the P1 region of a virulent variant of coxsackievirus B4 and the P2 and P3 regions of a nonvirulent strain was constructed from cDNA clones. The chimeric virus induced pancreatitis with concurrent hypoglycemia similar to that observed in mice infected with the virulent variant.
 ...
PMID:Evidence suggesting that virulence maps to the P1 region of the coxsackievirus B4 genome. 215 63

The presence of mumps virus and enterovirus RNA was studied by in situ hybridization in 15 surgical biopsy specimens from patients with acute pancreatitis. 35S-Labeled cRNA probes, detecting the 5' end of the poliovirus type 3, a 1.1-kb fragment of the polymerase gene region of coxsackievirus B3, and mumps virus mRNA, encoding the nucleocapsid protein, were used. The controls consisted of mumps virus-infected and uninfected cultured cells, normal human and mouse pancreatic tissue, and mouse tissue from experimental coxsackievirus B3-induced pancreatitis. No specific hybridization signal was observed in any of the acute pancreatitis cases. It is concluded that neither mumps virus nor enteroviruses tested were present in pancreatic tissue of advanced human acute pancreatitis.
 ...
PMID:Mumps, enteroviruses, and human acute pancreatitis. 217 Nov 34

DBA/2 male mice inoculated intraperitoneally with 1.8 X 10(5) plaque-forming units (PFU) coxsackievirus B-3 (CVB3) showed extensive inflammatory cell infiltration of the myocardium and acinar tissue of the pancreas in 7 days. Selective depletion of T lymphocyte subpopulations indicated that CD4 cells were either completely or partially responsible for cell damage in both organs. Other organs such as the liver were infected and contained virus titers equivalent to those seen in the heart and pancreas but showed no apparent tissue injury. The role of the CD4 cell was confirmed by positive selection of either T cell subpopulation from CVB3-immune lymphocytes in vitro and adoptive transfer of these cells into T cell-deficient (thymectomized, irradiated, bone marrow reconstituted, TXBM) DBA/2 recipients. Lymphocytes from CVB3-infected donor mice were adsorbed to myocyte, skin fibroblast, or liver vascular endothelial cell (VEC) monolayers. The adherent population was retrieved and adoptively transferred into uninfected syngeneic recipients. When killed 7 days later, the animals receiving unfractionated immune lymphocytes or cells eluted from heart monolayers developed both myocarditis and pancreatitis. Anti-Thy 1.2 and C' treatment of the unfractionated cells completely abrogated transfer of disease. Cells eluted from either fibroblast or liver VEC monolayers showed no pathogenicity. Adsorption of immune cells to heart monolayers in the presence of anti-IAd (class II major histocompatibility complex antigen, MHC) inhibited attachment of the pathogenic T cell, whereas anti KdDd (a class I MHC antigen) had no effect.
 ...
PMID:Coxsackievirus-induced disease. CD4+ cells initiate both myocarditis and pancreatitis in DBA/2 mice. 257 84

This report describes a patient on continuous ambulatory peritoneal dialysis (CAPD) who developed acute pancreatitis with pseudocyst formation and cloudy dialysate with pleocytosis in the absence of bacterial or fungal organisms. To our knowledge, pancreatitis, in the absence of hypertriglyceridemia in a CAPD patient, has not been previously reported. There was a significant increase in Coxsackie B1 and B6 viral titers by complement fixation test, suggesting Coxsackie virus-induced pancreatitis.
 ...
PMID:Coxsackie virus-induced acute pancreatitis in a long-term dialysis patient. 283 3

Thirty-seven clinical isolates of coxsackievirus (CV) serotypes B-1, B-3, B-4, and B-5 were inoculated into male SJL mice. Twelve strains resulted in minor abnormalities of glucose metabolism in one or more of six infected mice (Tables 1 and 2). Sequential infection of male SJL mice with CVB-3, CVB-4, and CVB-5 resulted in abnormal glucose metabolism in 25 percent of the mice (Fig. 1). The glucose index of the abnormal animals was similar to that produced by sequential infection with reovirus and cytomegalovirus but less than that seen with more severe beta cell tropic agents such as streptozotocin or encephalomyocarditis virus. Infection of autoimmune New Zealand (NZB X NZW) F1 male mice with CBV-3, CVB-4, and CVB-5 resulted in transient elevation of the blood glucose concentration associated with acute acinar pancreatitis (Fig. 2). In spite of recent evidence that infection with the coxsackie B viruses can result in human diabetes mellitus, the diabetogenic potential of CVB field strains appears to be limited. Diabetes mellitus may occur as a rare event, limited to genetically susceptible hosts. Autoimmune mechanisms or repeated infection with other CVB serotypes may convert minimal beta-cell destruction into clinically overt disease.
 ...
PMID:Diabetogenic potential of coxsackie B viruses in nature. 299

The pancreatic uptake of 99mTc stannous pyrophosphate (99mTc-PYP) in acute pancreatitis in mice induced by coxsackievirus B3 was studied. 99mTc-PYP uptake ratio, measured by the ratio of counts/min/g for the pancreas to counts/min/g for the skull, began to increase 2 days after virus inoculation and markedly increased on day 3 when necrosis of pancreatic acinar cells was evident. On day 5, 99mTc-PYP ratio reached a maximum (2.95 +/- 1.85, mean +/- SD) and histologically fine granules of calcification were seen in the necrotic acinar cells. Thereafter, cellular infiltrations increased and were most severe on day 7, but 99mTc-PYP ratio had began to decrease. On day 28, the necrotic areas of the pancreas were replaced with fatty cells and calcification was still present, though 99mTc-PYP ratio had decreased. The present findings may provide a basis for 99mTc-PYP imaging in cases of clinical viral pancreatitis.
 ...
PMID:Pancreatic uptake of 99Tc stannous pyrophosphate in experimental viral pancreatitis in mice. 626 May

Within a space of four months, between March to June 1993, medico-legal autopsies on 9 sudden infant deaths from natural causes were conducted at the Department of Forensic Medicine. Of these, 6 were due to unspecified interstitial pneumonitis or myocarditis (consistent with viral aetiologies), while 1 was attributed to adenovirus infection. The remaining 2 were due to fulminant Coxsackie virus (type B1) infection, where the post-mortem findings included leptomeningitis, myocarditis, florid interstitial pneumonitis, pancreatitis and focal hepatic necrosis. Coxsackie B viruses are often implicated in perinatal disease and, together with other viral infections, should be considered in the investigation of all sudden infant deaths.
 ...
PMID:Acute fulminant, fatal coxsackie B virus infection: a report of two cases. 774 14

Balb/c weanling mice were intraperitoneally inoculated with a myocarditic variant of coxsackievirus B3, with the aim of characterizing more thoroughly the features of virus-induced cell injury in pancreas and heart, as well as to compare ultrastructural alterations with histological and virological findings. During the first week post-infection (pi), all animals developed acinar pancreatitis, followed by focal myocarditis. At electron microscopy, acinar cells showed patent distortion, including marked loss of organelles and zymogen granules, together with gross dilatation of rough endoplasmic reticulum. Cardiac cells presented severe cytoskeletal changes, as myofibrillar collapse with a haphazard arrangement, concomitant with a decrease in myofibril number; besides, irregular pattern of nuclear chromatin and increased presence of swollen mitochondria were often observed. As the few initially detected lymphocytes tended to disappear in necrotic foci, there was an increase in fibroblast number concurrent with progressive scarring. Ultrastructural changes in both pancreas and heart correlated with local viral replication, suggesting that cell damage is attributable to direct viral action.
 ...
PMID:Ultrastructural study of cell injury induced by coxsackievirus B3 in pancreatic and cardiac tissues. 820 11

The ability of two coxsackievirus B3 (CBV3) variants to induce myocarditis in BALB/c mice was studied and plaque-forming assay, polymerase chain reaction (PCR), in situ hybridization, and immunohistochemistry were compared for detecting viruses and viral components in the myocardium. The virological findings were related to histopathologic and ultrastructural changes in the myocardium. CBV3-W induced severe myocarditis characterized by massive myocyte necrosis. Widely distributed myocyte damage clearly preceded modest inflammatory infiltrates in the myocardium. In contrast, CBV3-M1 induced mild myocardial injury. Both variants caused fulminant pancreatitis with nearly complete necrosis of the exocrine pancreas. CBV3 RNA was identified by PCR in the myocardium of CBV3-W-infected mice until the end of the follow-up period of 14 days. Moreover, semiquantitative results were obtained when the PCR/hybridization results were analyzed by a phosphor imaging system. Immunohistochemistry and in situ hybridization from formaldehyde-fixed, paraffin-embedded specimens were highly similar in detecting viral components during the early stages of the myocardial injury. The results indicate that: (i) direct viral damage plays an essential role in acute murine CBV3-induced myocarditis, (ii) PCR appears a useful and sensitive diagnostic method in acute myocarditis, and (iii) immunohistochemistry as a specific and relatively rapid method might be practicable also in studying the early stages of acute myocarditis from archival clinical material.
 ...
PMID:Experimental myocarditis induced by two different coxsackievirus B3 variants: aspects of pathogenesis and comparison of diagnostic methods. 855 Dec 77


1 2 3 4 5 Next >>