THE DEVELOPMENT OF INCLUSIONS IN TISSUE CULTURES OF MONKEY KIDNEY EPITHELIAL CELLS INFECTED WITH POLIOMYELITIS VIRUS

1956 ◽  
Vol 2 (3) ◽  
pp. 298-303 ◽  
Author(s):  
A. J. Beale ◽  
Patricia F. Stevens ◽  
Norma Davis ◽  
W. Stackiw ◽  
A. J. Rhodes
Keyword(s):  
Tissue Culture ◽  
Epithelial Cells ◽  
Inclusion Bodies ◽  
Cytoplasmic Inclusion ◽  
Monkey Kidney ◽  
Tissue Cultures ◽  
Cytoplasmic Inclusions ◽  
Poliomyelitis Virus ◽  
Eosinophilic Inclusion ◽  
Cytoplasmic Inclusion Body

A cytoplasmic inclusion body has been found in the epithelial cells of monkey kidney grown in tissue culture and infected with poliomyelitis virus. This inclusion is at first closely applied to the nucleus, and later develops into a clearly demarcated structure. The nucleus is pushed to the periphery of the cell and becomes pyknotic. Finally, the cytoplasm around the inclusion becomes vacuolated, and the cell breaks up at about the time virus first appears in the fluid part of the infected tissue cultures. Multiple small intranuclear eosinophilic inclusion bodies have also been found in some cells that contain cytoplasmic inclusions.

The Experimental Production of Goblet Cells and Inclusion Bodies

1947 ◽  
Vol s3-88 (3) ◽  
pp. 345-352
Author(s):  
E. MEIROWSKY ◽  
G. BEHR ◽  
S. KEYS
Keyword(s):  
Epithelial Cells ◽  
Inclusion Bodies ◽  
Goblet Cells ◽  
Experimental Production ◽  
Response Mechanism ◽  
Cytoplasmic Inclusions

1. Goblet cells have been produced experimentally in rabbits' and guineapigs' corneae by ten methods. 2. Goblet cells can develop from ordinary epithelial cells. 3. The secretion antecedents originate in the nucleus. 4. Intranuclear and cytoplasmic inclusions can be produced experimentally and form the response mechanism of the cell towards animate and inanimate stimuli.

scholarly journals INTERFERENCE BETWEEN POLIOMYELITIS VIRUSES IN TISSUE CULTURE

1954 ◽  
Vol 100 (3) ◽  
pp. 247-267 ◽  
Author(s):  
Nada Ledinko ◽  
Joseph L. Melnick
Keyword(s):  
Tissue Culture ◽  
Ultraviolet Light ◽  
High Energy ◽  
Coxsackie Virus ◽  
Complete Suppression ◽  
Tissue Cultures ◽  
Poliomyelitis Virus ◽  
Active Virus ◽  
High Energy Electrons ◽  
Homologous Virus

The inhibition of multiplication of one poliomyelitis virus by a poliomyelitis virus of another immunologic type has been established by using tissue cultures of monkey testes. The degree of interference varied from none, to partial, to complete, depending upon the time between inoculation of the interfering and the challenge viruses, and the amount of each virus inoculated. Reciprocal interference was demonstrated between Types 1, 2, and 3 poliomyelitis viruses. Under conditions which resulted in complete suppression of the growth of one poliomyelitis virus by another, interference by poliomyelitis virus with the multiplication of four antigenically distinct "orphan" viruses and of three antigenically related strains of Coxsackie virus could not be demonstrated. Poliomyelitis virus rendered non-infective by formalin or by irradiation with high energy electrons or with ultraviolet light, or treated so that only traces of residual active virus remained, failed to interfere with the propagation of active homologous virus.

Abstract 4: Macrophage p62/SQSTM1 Ameliorates Atherosclerosis by Sequestering Inclusion Bodies and Mediating Mitophagy

2015 ◽  
Vol 35 (suppl_1) ◽  
Author(s):  
Ismail Sergin ◽  
Somashubhra Bhattacharya ◽  
Carl J Stokes ◽  
John A Curci ◽  
Babak Razani
Keyword(s):  
Inclusion Bodies ◽  
Cytoplasmic Inclusion ◽  
Protein Aggregates ◽  
Whole Body ◽  
Plaque Burden ◽  
Protein Accumulation ◽  
Inflammasome Activation ◽  
Cytoplasmic Inclusions ◽  
Cytoplasmic Inclusion Bodies

Protein and organelle turnover is critical for cellular homeostasis and is prominently mediated by autophagy. Disruptions in autophagy lead to accumulation of protein aggregates and dysfunctional organelles such as mitochondria. Recent evidence suggests that the chaperone protein p62 is a critical link for targeting polyubiquitinated protein aggregates/damaged mitochondria to autophagosomes for degradation. Herein we describe a p62-centric mechanism of handling protein aggregates and dysfunctional mitochondria in atherosclerosis. Macrophages deficient in autophagy (ATG5-/-) or rendered deficient by incubation with atherogenic lipids have significantly increased levels of p62. This coincides with 1) the accumulation of polyubiquitinated proteins co-localizing with p62 and present as cytoplasmic inclusion bodies, and 2) p62 co-localization with mitochondrial markers. Aortas from atherosclerotic (ApoE-/-) mice also have progressive and marked elevations in p62, polyubiquitinated proteins, and mitochondrial reactive oxygen species that predominantly co-localize with plaque macrophages, a process further exacerbated in the autophagy-deficient setting. The formation of cytoplasmic inclusions and maintenance of adequate mitochondrial function appears to be dependent on p62. Lipid-loaded p62-null macrophages show polyubiquitinated protein accumulation present in a diffuse/disrupted cytoplasmic pattern. These macrophages also develop larger dysmorphic mitochondria with increased polarization and decreased oxidative phosphorylation capacity. As a result, p62-null macrophages display apoptotic susceptibility to atherogenic lipids and increased IL-1β secretion likely through mitochondrial-dependent inflammasome activation. Consistent with our in vitro observations, mice with either whole-body p62-deficiency or transplanted with p62-deficient bone marrow show significantly increased atherosclerotic plaque burden and lesion complexity with increased apoptosis and necrotic cores. Taken together, these data demonstrate a previously unrecognized atheroprotective role for macrophage p62 by facilitating the formation of inclusion bodies and maintaining healthy mitochondria.

scholarly journals Morphogenesis of Light and Electron Microscopic Lesions in Porcine GM2-Gangliosidosis

1979 ◽  
Vol 16 (1) ◽  
pp. 6-17 ◽  
Author(s):  
S. D. Kosanke ◽  
K. R. Pierce ◽  
W. K. Read
Keyword(s):  
Glial Cells ◽  
Inclusion Bodies ◽  
Cytoplasmic Inclusion ◽  
Particulate Material ◽  
Electron Microscopic ◽  
Cytoplasmic Body ◽  
Cytoplasmic Inclusions ◽  
Neuronal Inclusions ◽  
Cytoplasmic Inclusion Bodies ◽  
Cytoplasmic Structures

The neurons and glial cells of 1- to 140-day-old pigs with GM2-gangliosidosis had membranous cytoplasmic inclusion bodies. These bodies appeared as small vacuolated cytoplasmic structures in paraffin-embedded, hematoxylin and eosin-stained sections and as solid, dark, round granules in 1-micrometer sections embedded in plastic and stained with toluidine blue. Ultrastructurally, the cytoplasmic inclusion bodies appeared as round, dense structures from 0.6 to 1.2 micrometers in diameter, that were filled with various amounts of small to large arrays of membranous lamellae. The cortical neuronal inclusions were seen initially as lysosomes containing a small amount of particulate material. The appearance of these inclusions changed as they progressed through different configurational stages. Inclusions resembled the granulomembranous body, the zebra body, possibly other intermediate forms and, finally, the classical membranous cytoplasmic body. The cytoplasmic inclusions in glial cells resembled membranovesicular bodies and, although also of apparent lysosomal origin, were morphologically different from the neuronal inclusions. The morphologic lesions in the neurons and glial cells of the affected pigs were similar to those described for human gangliosidoses.

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