Acute Interstitial Pneumonia in Mink Kits: Experimental Reproduction of the Disease

1986 ◽  
Vol 23 (5) ◽  
pp. 579-588 ◽  
Author(s):  
S. Alexandersen

Organ homogenates from kits that died of interstitial pneumonia were inoculated into adult Aleutian disease virus (ADV)-negative mink and shown to contain infectious ADV. Acute interstitial pneumonia was experimentally reproduced with the organ homogenate but only by inoculation of newborn kits born from ADV-negative dams. Older kits and kits from ADV-positive dams did not develop interstitial pneumonia, but later developed the classic form of Aleutian disease. Electron microscopic examination was done on purified suspensions of defined ADV isolates and on purified organ homogenates from kits with spontaneous or experimental interstitial pneumonia. In kits from both groups a virus, morphologically resembling the defined ADV isolates, was demonstrated. Findings of intranuclear inclusion bodies and intranuclear ADV antigen in alveolar type-II cells in affected lungs and the lack of immunologically mediated lesions suggest that lung lesions result from primary viral injury to alveolar type-II cells. Experiments also showed that infection of dams with ADV before pregnancy decreased the number of kits per mated dam and infection with ADV in mid-pregnancy caused fetal death, fetal resorption, or abortion.

1991 ◽  
Vol 39 (2) ◽  
pp. 213-220 ◽  
Author(s):  
M Kalina ◽  
L Grimelius

Rat alveolar Type II cells were immunostained with antibodies directed against chromogranin A (monoclonal, LK2H10) and chromogranins A and B (polyclonal, LKZM1U). The chromogranins or chromogranin-like proteins were identified in cells in lung tissue sections and isolated Type II cells at the light and electron microscopic levels. We used post-embedding immunoelectron microscopy, with immunogold, to detect the proteins' immunoreactivity in osmicated tissues. Gold particles were distributed over the phospholipid lamellae within the lamellar bodies of alveolar Type II cells and over the lattice structure of tubular myelin. Quantitative analysis of gold labeling densities in the various cell compartments indicated that only the latter two structures were specifically labeled. Controls, which included pre-absorption of both anti-chromogranin antibodies with excess chromogranin A or with native surfactant, resulted in a greater than 60% decrease in gold labeling. A possible role of chromogranins or chromogranin-like proteins as Ca2+ binding proteins in alveolar Type II cells is discussed.


2018 ◽  
Vol 19 (8) ◽  
pp. 2203 ◽  
Author(s):  
Kazuhiro Osanai

Rab38 is highly expressed in alveolar type II cells, melanocytes, and platelets. These cells are specifically-differentiated cells and contain characteristic intracellular organelles called lysosome-related organelles, i.e., lamellar bodies in alveolar type II cells, melanosomes in melanocytes, and dense granules in platelets. There are Rab38-mutant rodents, i.e., chocolate mice and Ruby rats. While chocolate mice only show oculocutaneous albinism, Ruby rats show oculocutaneous albinism and prolonged bleeding time and, hence, are a rat model of Hermansky-Pudlak syndrome (HPS). Most patients with HPS suffer from fatal interstitial pneumonia by middle age. The lungs of both chocolate mice and Ruby rats show remarkably increased amounts of lung surfactant and conspicuously enlarged lysosome-related organelles, i.e., lamellar bodies, which are also characteristic of the lungs in human HPS. There are 16 mutant HPS-mouse strains, of which ten mutant genes have been identified to be causative in patients with HPS thus far. The gene products of eight of the ten genes constitute one of the three protein complexes, i.e., biogenesis of lysosome-related organelle complex-1, -2, -3 (BLOC-1, -2, -3). Patients with HPS of the mutant BLOC-3 genotype develop interstitial pneumonia. Recently, BLOC-3 has been elucidated to be a guanine nucleotide exchange factor for Rab38. Growing evidence suggests that Rab38 is an additional candidate gene of human HPS that displays the lung phenotype.


Respiration ◽  
1984 ◽  
Vol 46 (3) ◽  
pp. 303-309 ◽  
Author(s):  
Sanae Shimura ◽  
Shinsaku Maeda ◽  
Tamotsu Takismima

1986 ◽  
Vol 35 (24) ◽  
pp. 4537-4542 ◽  
Author(s):  
Tory M. Hagen ◽  
Lou Ann Brown ◽  
Dean P. Jones

1995 ◽  
Vol 23 (Supplement) ◽  
pp. A215
Author(s):  
Clark Williams ◽  
Wayne Ciesielski ◽  
Michelle Johns ◽  
Jerry Zimmerman

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