-
British Journal of Experimental... Jun 1976Infection of pregnant or non-pregnant mice with Coxsackieviruses B1, B3, B4 or B5 produced a severe pancreatitis consisting of a degeneration of the acinar cells, loss...
Infection of pregnant or non-pregnant mice with Coxsackieviruses B1, B3, B4 or B5 produced a severe pancreatitis consisting of a degeneration of the acinar cells, loss of zymogen granules, infiltration of mononuclear and plasma cells and a replacement of the exocrine tissue with fatty tissue. Coxsackieviruses B2 and B6 did not cause these changes in the period up to 6 weeks following virus injection. Suckling mice did not appear to be more susceptible to pancreatic damage due to these two viruses. Sequential studies on the development of Coxsackievirus B-induced pancreatic lesions indicated that although the changes due to B1, B3, B4 or B5 were similar in type, B3 and B4 exhibited a more rapid action in the tissue and more severe lesions than either B1 or B5. In this work, none of the Coxsackie B viruses examined elicited pathological changes in the islets of Langerhans detectable with the light microscope.
Topics: Animals; Coxsackievirus Infections; Female; Islets of Langerhans; Mice; Pancreas; Pancreatitis; Pregnancy; Pregnancy Complications, Infectious; Time Factors
PubMed: 782500
DOI: No ID Found -
The Journal of Infectious Diseases Jan 1980The susceptibility of mice to the diabetogenic effect of the M variant of encephalomyocarditis (MEMC) virus is probably inherited as a recissive trait. Three strains of...
The susceptibility of mice to the diabetogenic effect of the M variant of encephalomyocarditis (MEMC) virus is probably inherited as a recissive trait. Three strains of mice that were susceptible to MEMC virus, three strains that were not susceptible to MEMC virus, and three types of F1 hybrid strains were infected with the common human coxsackie virus, group B, type 4 (CB4). They were examined to determine the titer of virus and histochemistry in the pancreas, levels of blood glucose, urinalysis, glucose tolerance, and levels of plasma amylase and insulin. There was a positive correlation between MEMC virus-susceptibility (diabetes-prone) and CB4-induced beta cell degranulation with concurrent hyperinsulemia and hypoglycemia. Also, as for MEMC virus, the titer of CB4 in the pancreas was not genotype-dependent. However, there was an inverse relation between destruction of the exocrine pancreas and the effect on the endocrine pancreas. These results suggest that the genetic factors responsible for the effect of MEMC virus on the endocrine pancreas are also responsive to CB4, and the proposed recessive nature of these factors is maintained for both viruses. In contrast, these factors, which are operatively recessive traits for the effect of CB4 on the endocrine pancreas, appear to be expressed as dominant traits with respect to the exocrine pancreas.
Topics: Animals; Coxsackievirus Infections; Diabetes Mellitus, Experimental; Enterovirus B, Human; Genotype; Heterozygote; Insulin; Islets of Langerhans; Male; Mice; Mice, Inbred AKR; Mice, Inbred BALB C; Mice, Inbred C57BL; Mice, Inbred DBA; Pancreas
PubMed: 6245147
DOI: 10.1093/infdis/141.1.47 -
Toxicology Dec 2007Common viral infections have been shown to change the tissue distribution of xenobiotics, including polybrominated diphenyl ethers (PBDEs). In previous studies, it has...
Common viral infections have been shown to change the tissue distribution of xenobiotics, including polybrominated diphenyl ethers (PBDEs). In previous studies, it has been shown that CYP2B gene expression is induced after PBDE exposure whereas coxsackievirus B3 (CBV3) infection suppresses the expression of CYP-gene expression in the liver. In the present study, CVB3 adapted to Balb/c mice was used to study the combined effects of infection and exposure to pure BDE-99 or the commercial mixture Bromkal on CYP1A1 and CYP2B expression in the lungs and pancreas on day 3 of the infection. The quantitative gene expression of virus, CYP1A1 and CYP2B was measured by real-time polymerase chain reaction (RT-PCR). PBDE exposure in the non-infected mice tended to increase CYP2B expression in the lungs but not in the pancreas. Infection in both non-exposed and PBDE-exposed mice increased CYP2B expression in the lungs but was non-detectable in the pancreas. In the non-infected mice PBDE exposure left the CYP1A1 expression unaltered in both the lungs and pancreas. Infection in both non-exposed and PBDE-exposed mice tended to decrease the gene expression of CYP1A1 in the lungs but to induce it in the pancreas. A correlation between the amount of virus and the gene expression of CYP2B was found in the lungs. However, no effects of PBDE on virus replication were observed in any organ. In conclusion, viral infection affects CYP-gene expression differently in the pancreas and lungs whereas PBDE-induced effects were not obvious. The organ-specific change in gene expression could explain a changed tissue distribution of xenobiotics during infection.
Topics: Animals; Coxsackievirus Infections; Cytochrome P-450 CYP1A1; Cytochrome P-450 Enzyme System; Disease Models, Animal; Enterovirus B, Human; Female; Gene Expression Regulation, Enzymologic; Halogenated Diphenyl Ethers; Hydrocarbons, Brominated; Lung; Mice; Mice, Inbred BALB C; Pancreas; Phenyl Ethers; Reverse Transcriptase Polymerase Chain Reaction; Time Factors; Virus Replication
PubMed: 17964053
DOI: 10.1016/j.tox.2007.09.013 -
Nature Metabolism Feb 2021Infection-related diabetes can arise as a result of virus-associated β-cell destruction. Clinical data suggest that the severe acute respiratory syndrome coronavirus 2...
Infection-related diabetes can arise as a result of virus-associated β-cell destruction. Clinical data suggest that the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), causing the coronavirus disease 2019 (COVID-19), impairs glucose homoeostasis, but experimental evidence that SARS-CoV-2 can infect pancreatic tissue has been lacking. In the present study, we show that SARS-CoV-2 infects cells of the human exocrine and endocrine pancreas ex vivo and in vivo. We demonstrate that human β-cells express viral entry proteins, and SARS-CoV-2 infects and replicates in cultured human islets. Infection is associated with morphological, transcriptional and functional changes, including reduced numbers of insulin-secretory granules in β-cells and impaired glucose-stimulated insulin secretion. In COVID-19 full-body postmortem examinations, we detected SARS-CoV-2 nucleocapsid protein in pancreatic exocrine cells, and in cells that stain positive for the β-cell marker NKX6.1 and are in close proximity to the islets of Langerhans in all four patients investigated. Our data identify the human pancreas as a target of SARS-CoV-2 infection and suggest that β-cell infection could contribute to the metabolic dysregulation observed in patients with COVID-19.
Topics: Aged; Aged, 80 and over; Angiotensin-Converting Enzyme 2; COVID-19; Cells, Cultured; Diabetes Mellitus; Female; Humans; Islets of Langerhans; Male; Pancreas, Exocrine; Pancreatic Diseases; SARS-CoV-2; Serine Endopeptidases; Virus Internalization; Virus Replication
PubMed: 33536639
DOI: 10.1038/s42255-021-00347-1 -
Journal of Visceral Surgery Aug 2016The spleen and pancreas are at risk for injury during abdominal trauma. The spleen is more commonly injured because of its fragile structure and its position immediately... (Review)
Review
The spleen and pancreas are at risk for injury during abdominal trauma. The spleen is more commonly injured because of its fragile structure and its position immediately beneath the ribs. Injury to the more deeply placed pancreas is classically characterized by discordance between the severity of pancreatic injury and its initial clinical expression. For the patient who presents with hemorrhagic shock and ultrasound evidence of major hemoperitoneum, urgent "damage control" laparotomy is essential; if splenic injury is the cause, prompt "hemostatic" splenectomy should be performed. Direct pancreatic injury is rarely the cause of major hemorrhage unless a major neighboring vessel is injured, but if there is destruction of the pancreatic head, a two-stage pancreatoduodenectomy (PD) may be indicated. At open laparotomy when the patient's hemodynamic status can be stabilized, it may be possible to control splenic bleeding without splenectomy; it is always essential to search for injury to the pancreatic duct and/or the adjacent duodenum. Pancreatic contusion without ductal rupture is usually treated by drain placement adjacent to the injury; ductal injuries of the pancreatic body or tail are treated by resection (distal pancreatectomy with or without splenectomy), with generally benign consequences. For injuries of the pancreatic head with pancreatic duct disruption, wide drainage is usually performed because emergency PD is a complex gesture prone to poor results. Postoperatively, the placement of a ductal stent by endoscopic retrograde catheterization may be decided, while management of an isolated pancreatic fistula is often straightforward. Non-operative management is the rule for the trauma victim who is hemodynamically stable. In addition to the clinical examination and conventional laboratory tests, investigations should include an abdominothoracic CT scan with contrast injection, allowing identification of all traumatized organs and assessment of the severity of injury. In this context, non-operative management (NOM) has gradually become the standard as long as the patient remains hemodynamically stable and there is no suspicion of injury to hollow viscera, with the patient being carefully monitored on a surgical service. The development of arteriography with splenic artery embolization has increased the rate of splenic salvage; this can be performed electively based on specific indications (blush on CT, pseudoaneurysm, arteriovenous fistula), and may also be considered for severe splenic injury, abundant hemoperitoneum, or severe polytrauma. For pancreatic injury, in addition to CT scan, magnetic resonance pancreatography (MRCP) or even endoscopic retrograde cholangiopancreatography (ERCP) may be necessary to identify a ductal rupture. If the pancreatic duct is intact, laboratory and CT imaging surveillance is performed just as for splenic injury. In case of pancreatic ductal injury, ERCP stenting can be considered. However, if this is unsuccessful, the therapeutic decision can be difficult: while NOM can still be successful, complications may arise that are difficult to treat while distal pancreatectomy, although initially more agressive may avoid these complications if performed early.
Topics: Abdominal Injuries; Angiography; Embolization, Therapeutic; Hemoperitoneum; Humans; Infections; Laparotomy; Pancreas; Pancreaticoduodenectomy; Postoperative Complications; Spleen; Splenectomy
PubMed: 27402320
DOI: 10.1016/j.jviscsurg.2016.04.005 -
Khirurgiia 2014Approximately 24,000 people are infected with cat scratch disease (CSD) every year. CSD is caused by the bacteria Bartonella henselae, a gram-negative bacteria most...
Approximately 24,000 people are infected with cat scratch disease (CSD) every year. CSD is caused by the bacteria Bartonella henselae, a gram-negative bacteria most often transmitted to humans through a bite or scratch from an infected cat or kitten. Although CSD is often a benign and self-limiting condition, it can affect any major organ system in the body, manifesting in different ways and sometimes leading to lifelong sequelae. It is a disease that is often overlooked in primary care because of the wide range of symptom presentation and relative rarity of serious complications. It is important for health care providers to recognize patients at risk for CSD, know what laboratory testing and treatments are available, and be aware of complications that may arise from this disease in the future.
Topics: Adult; Bartonella henselae; Cat-Scratch Disease; Female; Granuloma; Hepatomegaly; Humans; Pancreas; Pancreatectomy; Radiography; Splenectomy; Splenomegaly; Treatment Outcome
PubMed: 25199244
DOI: No ID Found -
International Journal of Cardiology Aug 2016There is a clinical need for immunosuppressive therapy that can treat myocarditis patients in the presence of an active viral infection. In this study we therefore...
BACKGROUND
There is a clinical need for immunosuppressive therapy that can treat myocarditis patients in the presence of an active viral infection. In this study we therefore investigated the effects of colchicine, an immunosuppressive drug which has been used successfully as treatment for pericarditis patients, in a mouse model of coxsackievirus B3(CVB3)-induced myocarditis.
METHODS
Four groups of C3H mice were included: control mice (n=8), mice infected with CVB3 (1×10(5) PFU, n=10), mice with colchicine administration (2mg/kg i.p, n=5) and mice with combined CVB3 infection and colchicine administration (n=10). After three days, the heart, pancreas and spleen were harvested and evaluated using (immuno)histochemical analysis and CVB3 qPCR.
RESULTS
Mice were terminated at day 3 post-virus infection as colchicine treatment rapidly resulted in severe illness and mortality in CVB3-infected mice. Colchicine significantly decreased the number of macrophages in the heart in CVB3-infected mice (p<0.01) but significantly increased the number of neutrophils (p<0.01). In the pancreas, colchicine caused complete destruction of the acini in the CVB3-infected mice and also significantly decreased macrophage (p<0.01) and increased neutrophil numbers (p<0.01). In the spleen, colchicine treatment of CVB3-infected mice induced massive apoptosis in the white pulp and significantly inhibited the virus-induced increase of megakaryocytes in the spleen (p<0.001). Finally, we observed that colchicine significantly increased CVB3 levels in both the pancreas and the heart.
CONCLUSIONS
Colchicine treatment in CVB3-induced myocarditis has a detrimental effect as it causes complete destruction of the exocrine pancreas and enhances viral load in both heart and pancreas.
Topics: Animals; Colchicine; Coxsackievirus Infections; Disease Models, Animal; Enterovirus B, Human; Heart; Humans; Male; Mice; Mice, Inbred C3H; Myocarditis; Pancreas; Spleen; Treatment Outcome; Viral Load
PubMed: 27140338
DOI: 10.1016/j.ijcard.2016.04.144 -
Bailliere's Clinical Endocrinology and... Oct 1994The pancreas is frequently involved during HIV infection, especially by disseminated infections or neoplasms. These lesions are generally asymptomatic and are discovered... (Review)
Review
The pancreas is frequently involved during HIV infection, especially by disseminated infections or neoplasms. These lesions are generally asymptomatic and are discovered at autopsy. However, hypoglycaemia secondary to massive pancreatic infiltration by a tumour or tuberculous necrosis may occur. The most important cause of pancreatic dysfunction in HIV-infected patients is a drug toxic effect (intravenous pentamidine, didanosine, zalcitabine). Hypoglycaemia, which may or may not be followed by diabetes, can develop during intravenous pentamidine therapy. In cases with increased serum amylase and/or lipase levels, potentially toxic drugs must be promptly discontinued to avoid major pancreatic involvement.
Topics: AIDS-Related Opportunistic Infections; Acute Disease; Didanosine; HIV Infections; Humans; Pancreas; Pancreatic Diseases; Pancreatitis; Pentamidine; Trimethoprim, Sulfamethoxazole Drug Combination; Zalcitabine
PubMed: 7811227
DOI: 10.1016/s0950-351x(05)80306-4 -
Journal of Medical Primatology Jul 1994Following an experimental SIV infection, 11 rhesus monkeys were evaluated to determine the presence of opportunistic infections. Five animals had severe alterations of...
Following an experimental SIV infection, 11 rhesus monkeys were evaluated to determine the presence of opportunistic infections. Five animals had severe alterations of the hepatobiliary tree, three of which were associated with the presence of numerous Cryptosporidium spp. Subacute to chronic inflammatory changes were observed in the pancreatic ducts of four animals, one without histologic evidence of parasites. In one animal, the inflamed ducts were associated with a chronic interstitial pancreatitis. The rate of Cryptosporidium infection together with hepatic and pancreatic involvement (36%) supports the hypothesis that systemic cryptosporidiosis is the result of a loss of protective mucosal immunity.
Topics: Animals; Chronic Disease; Cryptosporidiosis; Cryptosporidium; Liver; Macaca mulatta; Opportunistic Infections; Pancreas; Pancreatic Ducts; Pancreatitis; Simian Acquired Immunodeficiency Syndrome
PubMed: 7869359
DOI: 10.1111/j.1600-0684.1994.tb00288.x -
Transplantation Aug 2005Whether peritoneal dialysis is a risk factor for the development of intra-abdominal infection (IAI) after simultaneous pancreas kidney (SPK) transplantation is...
BACKGROUND
Whether peritoneal dialysis is a risk factor for the development of intra-abdominal infection (IAI) after simultaneous pancreas kidney (SPK) transplantation is controversial.
METHODS
We investigated the incidence of IAI, and patient and pancreas graft survival rates of 120 patients that received SPK between November 1995 and August 2003. All patients were dialysis-dependent prior to transplantation; mean duration of peritoneal dialysis (PD; n=52) and hemodialysis (HD; n=68) was 20+/-15 months and 23+/-16 months, respectively.
RESULTS
IAI developed in five PD and six HD patients (P=0.88). The time of diagnosis of IAI and the spectrum of organisms cultured were similar in the two groups of patients. Age, duration of dialysis, and method of exocrine drainage did not have a significantly impact on infection rate. Patient and pancreas graft survival rates were 92.3% and 88.4% in the PD group and 95.5% and 92% HD group (p=ns) after a mean follow-up of 42+/-27 months and 39+/-27 months, respectively. Overall patient and pancreas graft survival was not significantly affected by IAI.
CONCLUSIONS
PD does not adversely affect IAI rate and is a safe mode of dialysis for patients awaiting SPK transplantation.
Topics: Adult; Anti-Infective Agents; Female; Humans; Infections; Kidney Transplantation; Male; Pancreas; Pancreas Transplantation; Peritoneal Dialysis; Peritoneum; Postoperative Complications; Renal Dialysis; Risk Factors; Time Factors; Treatment Outcome
PubMed: 16082329
DOI: 10.1097/01.tp.0000168150.42491.37