Morphological Characteristics of Infectious Pancreatic Necrosis Yirus in Trout Pancreatic Tissue

1969 ◽  
Vol 26 (8) ◽  
pp. 2247-2250 ◽  
Author(s):  
Donald Lightner ◽  
George Post
Keyword(s):  
Pancreatic Necrosis ◽  
Morphological Characteristics ◽  
Acinar Cells ◽  
Pancreatic Tissue ◽  
Pancreatic Acinar Cells ◽  
Salmo Gairdneri ◽  
Thin Sections ◽  
Virus Particles ◽  
Infectious Pancreatic Necrosis ◽  
Electron Microscopical

Electron microscopical observations were made of infectious pancreatic necrosis (IPN) virus in thin sections of pancreatic acinar cells of rainbow trout (Salmo gairdneri). The virus and trout used in this study were obtained from a naturally occurring IPN epizootic in Colorado trout hatcheries and rearing units in 1968. IPN virus particles were found in large numbers in pancreatic acinar cells. Virus particles were associated most often with inclusion bodies composed of masses of virus particles and cell debris or large crystalline aggregations that were encircled by a single-layered membrane. Mature virus particles were found to average 57 nm in diameter and were hexagonal in profile.

scholarly journals Membrane interactions between secretion granules and plasmalemma in three exocrine glands

1980 ◽  
Vol 84 (2) ◽  
pp. 438-453 ◽  
Author(s):  
Y Tanaka ◽  
P De Camilli ◽  
J Meldolesi
Keyword(s):  
Plasma Membranes ◽  
Intact Cell ◽  
Freeze Fracture ◽  
Acinar Cells ◽  
Pancreatic Acinar Cells ◽  
Secretory Cells ◽  
Membrane Interactions ◽  
Thin Sections ◽  
Secretion Granules

Three types of membrane interactions were studied in three exocrine systems (the acinar cells of the rat parotid, rat lacrimal gland, and guinea pig pancrease) by freeze- fracture and thin-section electron microscopy: exocytosis, induced in vivo by specific pharmacological stimulations; the mutual apposition of secretory granule membranes in the intact cell; membrane appositions induced in vitro by centrifugation of the isolated granules. In all three glandular cells, the distribution of intramembrane particles (IMP) on the fracture faces of the luminal plasmagranule membrane particles (IMP) on the fracture faces of the lumenal plasmalemma appeared random before stimulation. However, after injection of secretagogues, IMP were rapidly clearly from the areas of granule- plasmalemma apposition in the parotid cells and, especially, in lacrimocytes. In the latter, the cleared areas appeared as large bulges toward the lumen, whereas in the parotid they were less pronounced. Exocytotic openings were usually large and the fracture faces of their rims were covered with IMP. In contrast, in stimulated pancreatic acinar cells, the IMP distribution remained apparently random after stimulation. Exocytoses were established through the formation of narrown necks, and no images which might correspond to early stages of membrane fusion were revealed. Within the cytoplasm of parotid and lacrimal cells (but not in the pancreas), both at rest and after stimulation, secretion granules were often closely apposed by means of flat, circular areas, also devoid of IMP. In thin sections, the images corresponding to IMP-free areas were close granule-granule and granule-plasmalemma appositions, sometimes with focal merging of the membrane outer layers to yield pentalaminar structures. Isolated secretion granules were forced together in vitro by centrifugation. Under these conditions, increasing the centrifugal force from 1,600 to 50,000 g for 10 min resulted in a progressive, statistically significant increase of the frequency of IMP-free flat appositions between parotid granules. In contrast, no such areas were seen between freeze-fractured pancreatic granules, although some focal pentalaminar appositions appeared in section after centrifugation at 50 and 100,000 g for 10 min. On the basis of the observation that, in secretory cells, IMP clearing always develops in deformed membrane areas (bulges, depressions, flat areas), it is suggested that it might result from the forced mechanical apposition of the interacting membranes. This might be a preliminary process not sufficient to initiate fusion. In the pancreas, IMP clearing could occur over surface areas too small to be detected. In stimulated parotid and lacrimal glands they were exceptional. These structures were either attached at the sites of continuity between granule and plasma membranes, or free in the acinar lumen, with a preferential location within exocytotic pockets or in their proximity. Experiments designed to investigate the nature of these blisters and vesicles revealed that they probably arise artifactually during glutaraldehyde fixation. In fact, (a) they were large and numerous in poorly fixed samples but were never observed in thin sections of specimens fixed in one step with glutaraldehyde and OsO(4); and (b) no increase in concentration of phospholipids was observed in the parotid saliva and pancreatic juice after stimulation of protein discharge, as was to be expected if release of membrane material were occurring after exocytosis.

Susceptibility of Trouts of Different Species and Origins to Various Isolates of Infectious Pancreatic Necrosis Virus

1982 ◽  
Vol 39 (12) ◽  
pp. 1580-1584 ◽  
Author(s):  
A. Silim ◽  
M. A. S. Y. Elazhary ◽  
A. Lagacé
Keyword(s):  
Rainbow Trout ◽  
Brook Trout ◽  
Pancreatic Necrosis ◽  
Lake Trout ◽  
Infectious Pancreatic Necrosis Virus ◽  
Infected Fish ◽  
Salmo Gairdneri ◽  
Necrosis Virus ◽  
Infectious Pancreatic Necrosis ◽  
Pancreatic Necrosis Virus

We investigated the susceptibility of trouts of different species and origins to infectious pancreatic necrosis virus (IPNV) and the pathogenicity of three strains of IPNV for brook trout (Salvelinus fontinalis) of various origins and lake trout (Salvelinus namaycush) of a single origin. Fish were inoculated by immersion in water containing 105 PFU of virus/mL for 6 h. Susceptibility to IPNV infection was assessed by counting dead fish over a period of 21 d after infection and on histological lesions in the pancreas, kidney, and intestine of the infected fish. Different species of trouts had different susceptibility to IPNV strain 3865. Brook trout had the highest mortality followed by rainbow trout (Salmo gairdneri), whereas the least mortality occurred in lake trout. Brook trout from Crowford, Nebraska, were more than twice as susceptible as the same species from Baldwin Mills, Quebec. Rainbow trout also varied in susceptibility as a result of origin. Virus isolate 3B, originally isolated from chain pickerel (Esox niger), was less virulent than isolates 4495 or 3865 (both from trout). Hatcheries that use water from sources containing pickerel may increase their chances of IPN infection.Key words: trout species, infectious pancreatic necrosis virus, resistance

scholarly journals Impaired autophagy increases susceptibility to endotoxin-induced chronic pancreatitis

2020 ◽  
Vol 11 (10) ◽  
Author(s):  
L. Xia ◽  
Z. Xu ◽  
X. Zhou ◽  
F. Bergmann ◽  
N. Grabe ◽  
...  
Keyword(s):  
Chronic Pancreatitis ◽  
Lethal Dose ◽  
Acinar Cells ◽  
Pancreatic Injury ◽  
Pancreatic Tissue ◽  
Pancreatic Acinar Cells ◽  
Chromogenic Assay ◽  
Enhanced Expression ◽  
Metabolic Endotoxemia

Abstract Chronic pancreatitis (CP) is associated with elevated plasma levels of bacterial lipopolysaccharide (LPS) and we have demonstrated reduced acinar cell autophagy in human CP tissue. Therefore, we investigated the role of autophagy in experimental endotoxin-induced pancreatic injury and aimed to identify LPS in human CP tissue. Pancreatic Atg7-deficient mice were injected with a single sub-lethal dose of LPS. Expression of autophagy, apoptosis, necroptosis, and inflammatory markers was determined 3 and 24 h later utilizing immunoblotting and immunofluorescence. The presence of LPS in pancreatic tissue from mice and from patients and healthy controls was determined using immunohistochemistry, immunoblots, and chromogenic assay. Mice lacking pancreatic autophagy exhibited local signs of inflammation and were particularly sensitive to the toxic effect of LPS injection as compared to control mice. In response to LPS, Atg7Δpan mice exhibited enhanced vacuolization of pancreatic acinar cells, increase in TLR4 expression coupled to enhanced expression of NF-κΒ, JNK, and pro-inflammatory cytokines by acinar cells and enhanced infiltration by myeloid cells (but not Atg7F/F controls). Cell death was enhanced in Atg7Δpan pancreata, but only necroptosis and trypsin activation was further amplified following LPS injection along with elevated pancreatic LPS. The presence of LPS was identified in the pancreata from all 14 CP patients examined but was absent in the pancreata from all 10 normal controls. Altogether, these results support a potential role for metabolic endotoxemia in the pathogenesis of CP. Moreover, the evidence also supports the notion that autophagy plays a major cytoprotective and anti-inflammatory role in the pancreas, and blunting metabolic endotoxemia-induced CP.

Electrogenic sodium pump in pancreatic acinar cells

1973 ◽  
Vol 184 (1074) ◽  
pp. 115-119 ◽  
Keyword(s):  
Cell Membrane ◽  
Acinar Cell ◽  
Sodium Pump ◽  
Acinar Cells ◽  
Pancreatic Tissue ◽  
Pancreatic Acinar Cells ◽  
Bathing Solution ◽  
Sodium Pumps ◽  
Epithelial Tissues ◽  
Electrogenic Sodium Pump

Electrogenic sodium pumps have been described in many excitable tissues, but hitherto not with certainty in epithelial tissues. In the present work it is shown that readmission of potassium to the bathing solution of mouse pancreatic tissue previously deprived of potas­sium, causes a marked hyperpolarization of the acinar cell membrane. This hyperpolariza­tion is abolished reversibly by strophanthin-G. This indicates the presence of electrogenic sodium pumping in pancreatic acinar cells.

Infectious Pancreatic Necrosis Virus Occurrence at a Hatchery in Alberta

1974 ◽  
Vol 31 (4) ◽  
pp. 397-402 ◽  
Author(s):  
T. Yamamoto
Keyword(s):  
Brook Trout ◽  
Pancreatic Necrosis ◽  
Salvelinus Fontinalis ◽  
Kidney Tissue ◽  
Infectious Pancreatic Necrosis Virus ◽  
Salmo Gairdneri ◽  
Necrosis Virus ◽  
High Incidence ◽  
Infectious Pancreatic Necrosis ◽  
Pancreatic Necrosis Virus

The presence of infectious pancreatic necrosis (IPN) virus in brook (Salvelinus fontinalis) and rainbow (Salmo gairdneri) trout was identified and further investigated. A high incidence of virus was found by virological examination of kidney tissue from yearling and older trout. By comparison, brook trout had a much higher incidence of virus than rainbow trout.The virus was isolated most frequently from the kidneys of both species of trout. These findings indicate that the examinations of peritoneal washes and feces is not adequate for the detection of IPN carrier fish.

Critical role for NHE1 in intracellular pH regulation in pancreatic acinar cells

2003 ◽  
Vol 285 (5) ◽  
pp. G804-G812 ◽  
Author(s):  
David A. Brown ◽  
James E. Melvin ◽  
David I. Yule
Keyword(s):  
Intracellular Ph ◽  
Ph Regulation ◽  
Critical Role ◽  
Acinar Cells ◽  
Pancreatic Tissue ◽  
Pancreatic Acinar Cells ◽  
Muscarinic Agonist ◽  
Targeted Disruption ◽  
General Role ◽  
Pancreatic Acini

The primary function of pancreatic acinar cells is to secrete digestive enzymes together with a NaCl-rich primary fluid which is later greatly supplemented and modified by the pancreatic duct. A Na+/H+ exchanger(s) [NHE(s)] is proposed to be integral in the process of fluid secretion both in terms of the transcellular flux of Na+ and intracellular pH (pHi) regulation. Multiple NHE isoforms have been identified in pancreatic tissue, but little is known about their individual functions in acinar cells. The Na+/H+ exchange inhibitor 5-( N-ethyl- N-isopropyl) amiloride completely blocked pHi recovery after an NH4Cl-induced acid challenge, confirming a general role for NHE in pHi regulation. The targeted disruption of the Nhe1 gene also completely abolished pHi recovery from an acid load in pancreatic acini in both [Formula: see text]-containing and [Formula: see text]-free solutions. In contrast, the disruption of either Nhe2 or Nhe3 had no effect on pHi recovery. In addition, NHE1 activity was upregulated in response to muscarinic stimulation in wild-type mice but not in NHE1-deficient mice. Fluctuations in pHi could potentially have major effects on Ca2+ signaling following secretagogue stimulation; however, the targeted disruption of Nhe1 was found to have no significant effect on intracellular Ca2+ homeostasis. These data demonstrate that NHE1 is the major regulator of pHi in both resting and muscarinic agonist-stimulated pancreatic acinar cells.

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