Identification and impact of hepatitis B virus DNA and antigens in pancreatic cancer tissues and adjacent non-cancerous tissues.

Increasing evidence suggests that a link exists between hepatitis B virus (HBV) serum markers and pancreatic cancer (PC). In this study, HBsAg and HBcAg were expressed in 21.0% (34/162) of PC and 29.0% (47/162) of non-tumor pancreatic tissues, and they were significantly associated with chronic pancreatitis (P=0.000). The HBV S, C and X genes were identified in 20% (6/30) of PC and 26.9% (7/26) of non-tumor tissues by PCR. A serological survey revealed that the prevalence of HBV DNA and anti-HBc was significantly increased in PC patients compared with healthy controls. Our data suggest that HBV infection in the pancreas may play an etiologic role in PC.

Dynamics of molecular responses to coxsackievirus B4 infection differentiate between resolution and progression of acute pancreatitis.

A coxsackievirus B4 induces acute pancreatitis with different outcomes. The study utilized a systems biology approach to identify molecular immune responses that differentiate between disease resolution and disease progression. The data establish a temporal pattern of host responses that differentiate the resolution of acute pancreatitis from the progression to chronic pancreatitis. A group of twenty-five genes exhibited characteristic expression profiles that were observed during the development of chronic pancreatitis but not during the resolution of disease. We postulate that the temporal dynamics of the twenty-five genes influence the development of pathogenic immune responses associated with chronic pancreatitis. Furthermore, a subset of eleven genes exhibited increased expression as viral titers waned. Of the eleven gene products, five are secreted molecules, TNF-α, IFN-γ, CXCL10, IL-10, and IL-22b, and represent novel potential therapeutic targets since they can be readily modulated with antibodies against the specific cytokine/chemokine or with antibodies against the corresponding receptors.

[Effectivity of detoxification preparation reamberin in complex treatment of the patients with chronic cholecystitis combined with chronic pancreatitis on background of HCV-infection].

Effectivity of detoxic preparation reamberin at complex treatment of the patients with acuting of chronic cholecystitis combined with chronic pancreatitis on background of HCV-infection was detected. It was set that before treatment took place increase "average molecules", lipid peroxidation products--malondialdehyde and dien conjugates and increase of circulatory immune complexes in serum. Including of reamberin provided to normalization clinical-biochemical indexes.

IL-10 is pathogenic during the development of coxsackievirus B4-induced chronic pancreatitis.

Using a mouse model of coxsackievirus B4 (CVB4-V)-induced chronic pancreatitis, we investigated whether cytokines are involved in the progression of acute disease to chronic inflammatory disease. We show that IL-10 contributed to the development of chronic pancreatitis since acute disease resolved when IL-10 was absent or when IL-10 signaling was disrupted. We explored the underlying mechanisms by which IL-10 affected disease progression, using a novel approach to assess immunological events occurring in situ. Multiple markers that define functional innate immune responses and functional T cell responses were monitored over the course of CVB4-V infection of wild-type and IL-10 knockout mice, using a multiplex transcriptional profiling approach. We show that high levels of IL-10 early during infection were associated with delayed innate and T cell responses. Furthermore, high IL-10 production correlated with altered kinetics of T regulatory responses indicating a disruption in the balance between effector and regulatory T cell responses.

CVB-induced pancreatitis and alterations in gene expression.

While infections with the group B coxsackieviruses are generally asymptomatic, these viruses occasionally cause acute and chronic inflammatory diseases of the pancreas and heart. Chronic inflammatory diseases are of major clinical concern, since they predispose affected individuals to cancer. For example, chronic pancreatitis, which can develop from acute pancreatitis, is a major risk factor for pancreatic cancer, a disease with an exceedingly poor prognosis. It is crucial that we understand the mechanisms underlying the development of acute pancreatitis and the progression to chronic disease, if we are to identify new therapeutic targets to prevent the deterioration of the exocrine pancreas. We have developed a mouse model that allows us to explore the mechanisms by which CVB4 causes acute and chronic pancreatitis. The present review develops the idea that disease progression is a continuum, from acute inflammatory disease to chronic inflammatory disease to cancer, and that accompanying changes in gene expression are both quantitative and qualitative.

Endocrine pancreatic insufficiency secondary to chronic herpesvirus pancreatitis in a cockatiel (Nymphicus hollandicus).

A cockatiel (Nymphicus hollandicus) examined because of weight loss, polydipsia, and polyuria was diagnosed with diabetes mellitus based on the presence of glucosuria and marked hyperglycemia. Medical attempts to manage the diabetes mellitus were unsuccessful, and the bird was euthanatized. Histopathologic examination of the pancreas revealed a chronic active pancreatitis with herpesviral inclusions in many of the pancreatic acinar and duct cells. Psittacid herpesvirus-1 (PsHV-1) DNA was amplified from the lesion by polymerase chain reaction. Sequencing of the amplicon showed it to be the genotype 1 variant, which is most commonly associated with Pacheco's disease, an acute rapidly fatal systemic infection. The findings in this case suggest that the PsHV-1 genotype may also cause a localized disease of the pancreas. Infection with this virus should be considered as a differential diagnosis in birds with pancreatitis with or without diabetes mellitus.