Differentiation and Cell Proliferation Patterns in Rat Exocrine Pancreas: Role of Type I and Type II Injury

Ms, Rao; Av, Yeldandi; Jk, Reddy

doi:10.1159/000163563

Cited by 16 publications

(8 citation statements)

References 24 publications

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“…The mechanism of pancreatic regeneration is not well understood. It appears that the magnitude of the regenerative response is dependent on the extent of acinar cell necrosis (25). In addition, the tubular or ductular structures, sometimes referred to as pseudoductules (25), are thought to be involved in the repair process.…”

Section: Overview Of Pancreatitismentioning

confidence: 99%

“…It appears that the magnitude of the regenerative response is dependent on the extent of acinar cell necrosis (25). In addition, the tubular or ductular structures, sometimes referred to as pseudoductules (25), are thought to be involved in the repair process. Understanding the genesis and ultimate fate of the ductular structures is important since the presence of such structures is a well-documented phenomenon in a variety of human pancreatic diseases including pancreatitis, cystic fibrosis and pancreatic cancers (26)(27)(28)(29).…”

Section: Overview Of Pancreatitismentioning

confidence: 99%

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Coxsackieviruses and pancreatitis

Ramsingh

1997

Front Biosci

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While alcohol abuse and biliary disease can result in the development of pancreatitis, the factors that contribute to the idiopathic form of the disease are not well understood. I propose that coxsackievirus infections account for a subset of cases of pancreatitis of unknown etiology. Evidence to support this concept is derived from serological studies, case reports and animal models. In reviewing the available data, it is obvious that the relationship between coxsackievirus infection and the development of pancreatitis is not a simple one. Many elements contribute to the development of the disease including the strain of the infecting virus, the genetic predisposition of the host and additional environmental factors that maintain the disease process. Studies that show an association between coxsackievirus infection and acute pancreatitis in humans are given additional support by the extensive data from mouse studies demonstrating that some serotypes (B4,B3) are tropic for the exocrine pancreas. Some viral strains may cause limited pancreatic tissue injury which is compatible with tissue repair followed by full restoration of pancreatic function. Other viral strains may cause more extensive tissue damage giving rise to chronic pancreatitis which, on a genetic background that predisposes to autoimmunity, may result in an autoimmune chronic pancreatitis. A multi-disciplinary approach is required to increase our understanding of the complex relationship between coxsackievirus infection and pancreatic diseases. Such studies should address the biology of viral replication, the immune response to infection, the role of viruses in the development of autoimmunity, the biology of pancreatic tissue injury and the underlying repair process.

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Section: Overview Of Pancreatitismentioning

confidence: 99%

Section: Overview Of Pancreatitismentioning

confidence: 99%

Coxsackieviruses and pancreatitis

Ramsingh

1997

Front Biosci

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“…Formation of ductlike struc-Wiberg, Saari, and Westermarck tures, defined as tubular complexes, can occur as a general reaction to the destruction of acinar cells in various types of injury: in acute and chronic pancreatitis, after pancreatic duct ligation, in pancreatic carcinoma, and in metabolic and nutritional disorders. 4,5,18,27,34,36 In the case of mild injury, tubular complexes can be reversible, but after severe injury, such as in chronic pancreatitis, the changes are usually irreversible. 18,27 Recent evidence has shown that tubular complexes are formed by acinar cells showing varying levels of dedifferentation.…”

Section: Discussionmentioning

confidence: 99%

Exocrine Pancreatic Atrophy in German Shepherd Dogs and Rough-coated Collies: An End Result of Lymphocytic Pancreatitis

Wiberg

Saari

Westermarck³

1999

Vet Pathol

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Abstract. Previously published studies of the pathology of canine exocrine pancreatic insufficiency (EPI) have been based on morphological findings during the clinical phase of the disease, when atrophy of acinar parenchyma occurs. Recently, low serum trypsinlike immunoreactivity (TLI) concentration has been shown to precede clinical signs, making it possible to diagnose EPI prior to onset of the clinical disease. This study presents histological and ultrastructural findings of pancreatic biopsies from 11 German Shepherd Dogs and 2 Rough-coated Collies with subclinical EPI (SEPI). These findings were compared with those from dogs with clinical EPI (n ϭ 11) and healthy control dogs (n ϭ 5). Biopsied tissue from dogs with SEPI typically contained both normal and atrophied acinar parenchyma. The most significant finding was the marked lymphocytic infiltration, which was most prevalent at the border zone of affected and nonaffected parenchyma but had spread into the normal acinar tissue. Numerous intraacinar lymphocytes were found. Most of the lymphocytes were positive by immunostaining for CD3. In more advanced stages of destruction, the findings were characteristic of pancreatic acinar atrophy. In the atrophied parenchyma, the inflammatory reaction, if present, was less prominent. Ultrastructural changes were in accordance with those of the histological study showing infiltration of lymphocytes both in affected acini and in acini that revealed no obvious ultrastructural changes. Progressive degenerative changes of acinar cells were considered a nonspecific finding. Apoptotic death of acinar cells was occasionally found. The inflammatory reaction was clearly shown to precede the pancreatic acinar atrophy, and the findings suggested that lymphocytic pancreatitis leads to atrophy of the pancreas. The possibility that EPI is an immune-mediated disease in German Shepherd Dogs and Rough-coated Collies is discussed.

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“…Numerous ductular structures suggestive of acinoductular metaplasia were apparent. The presence of tubular/ductular complexes, also referred to as pseudoductules (26), in a variety of pancreatic diseases, including pancreatitis, cystic fibrosis, and pancreatic cancers, is well documented (19)(20)(21)33). The presence of these ductular complexes may reflect the extent of acinar injuries (26).…”

Section: Viral Replication In Vivomentioning

confidence: 99%

“…The presence of tubular/ductular complexes, also referred to as pseudoductules (26), in a variety of pancreatic diseases, including pancreatitis, cystic fibrosis, and pancreatic cancers, is well documented (19)(20)(21)33). The presence of these ductular complexes may reflect the extent of acinar injuries (26). Extensive tissue injury, associated with CB4-V infection, correlated with numerous ductular structures, while lesser injury observed with CB4-P infection correlated with very few ductular structures.…”

Section: Viral Replication In Vivomentioning

confidence: 99%

Differential recruitment of B and T cells in coxsackievirus B4-induced pancreatitis is influenced by a capsid protein

Ramsingh

Lee

Collins

et al. 1997

J Virol

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Two genetically similar variants of coxsackievirus B4, CB4-P and CB4-V, cause distinct disease syndromes in mice. A multidisciplinary approach was used to examine the events occurring in situ. The CB4-P variant induced acute pancreatitis, followed by repair of the exocrine tissues, while the CB4-V variant induced chronic pancreatitis, characterized by extensive destruction of the exocrine tissues. Since CB4-V replicated more efficiently than CB4-P in vivo, the more extensive tissue injury associated with CB4-V infection could be explained as the result of a higher level of viral replication. However, the fact that CB4-V replicated more efficiently in a mouse strain that survives infection than in a strain that succumbs to infection suggests that immune-mediated mechanisms as well as viral cytolysis may contribute to pancreatic tissue injury. To address the role of the immune system in virus-induced pancreatitis, the cell types within the inflammatory infiltrate were analyzed by flow cytometry. B cells (34 to 75%) were the most abundant, followed by T cells (10 to 30%), natural killer cells (4 to 8%), and macrophages (0 to 6%). Recruitment (and perhaps proliferation) of B and T cells to the pancreatic tissues was influenced by viral strain. Differential recruitment of T and B cells may reflect altered antigenic sites between CB4-P and CB4-V. The viral sequence that affected T-and B-cell recruitment was identified as a threonine residue at position 129 of the VP1 capsid protein.

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Differentiation and Cell Proliferation Patterns in Rat Exocrine Pancreas: Role of Type I and Type II Injury

Cited by 16 publications

References 24 publications

Coxsackieviruses and pancreatitis

Coxsackieviruses and pancreatitis

Exocrine Pancreatic Atrophy in German Shepherd Dogs and Rough-coated Collies: An End Result of Lymphocytic Pancreatitis

Differential recruitment of B and T cells in coxsackievirus B4-induced pancreatitis is influenced by a capsid protein

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