scholarly journals THE INFLUENCE OF CORTISONE ON EXPERIMENTAL VIRAL INFECTION

1966 ◽  
Vol 123 (2) ◽  
pp. 309-325 ◽  
Author(s):  
K. Marilyn Smart ◽  
Edwin D. Kilbourne
Keyword(s):  
Chick Embryo ◽  
Inflammatory Response ◽  
Chorioallantoic Membrane ◽  
Allantoic Fluid ◽  
Influenza Viruses ◽  
Present System ◽  
Interferon Production ◽  
Hydrocortisone Administration ◽  
Experimental Viral Infection

A comparative study was undertaken of the pathogenesis of infection of the allantoic sac of the chick embryo with three influenza viruses of differing virulence, and of the influence of hydrocortisone on the course of infection. Judged on the basis of earlier onset and greater degree of inflammatory response and diminished survival time of infected embryos, Mel. and Lee viruses were markedly more virulent than PR8, despite the earlier appearance of virus in PR8-infected embryos. Interferon appeared first and in greater quantity in the allantoic fluid of Lee-infected embryos and latest with PR8 infection. Thus, there was no correlation of avirulence and better interferon production with the viruses under study in the present system. Furthermore, evidence obtained suggested that Lee virus ("virulent") was most susceptible to interferon action, and also that viral synthesis in the chorioallantoic membrane with PR8 ("avirulent") persisted after the appearance of interferon. The injection of hydrocortisone within 2 hr of the initiation of infection delayed the synthesis of all three viruses; had no significant effect upon the inflammatory response; and transiently inhibited the synthesis of interferon, while prolonging the survival of Lee- and Mel.-infected embryos. Late administration of hydrocortisone suppresses both the inflammatory response and the production of interferon. Only in the case of Lee virus infection did hydrocortisone administration lead to augmentation of final yields of virus with the low infection multiplicity employed in the present experiments. It is postulated that Lee virus is a better inducer of interferon because its infectivity in vivo is more rapidly inactivated. As a consequence synthesis of Lee virus is more under the control of endogenous interferon than is the case with PR8 or Mel. virus. Therefore, inhibition of interferon synthesis with hydrocortisone has a greater influence on final yields of Lee virus.

The Chick Embryo Chorioallantoic Membrane as an in vivo Wound Healing Model

1996 ◽  
Vol 192 (10) ◽  
pp. 1068-1076 ◽  
Author(s):  
D. Ribatti ◽  
A. Vacca ◽  
G. Ranieri ◽  
S. Sorino ◽  
L. Roncali
Keyword(s):  
Wound Healing ◽  
Chick Embryo ◽  
Chorioallantoic Membrane ◽  
Chick Embryo Chorioallantoic Membrane ◽  
Wound Healing Model ◽  
Healing Model

scholarly journals The Chick Embryo Chorioallantoic Membrane as a Model for in vivo Research on Anti-Angiogenesis

2000 ◽  
Vol 1 (1) ◽  
pp. 73-82 ◽  
Author(s):  
Domenico Ribatti ◽  
Angelo Vacca ◽  
Luisa Roncali ◽  
Franco Dammacco
Keyword(s):  
Chick Embryo ◽  
Chorioallantoic Membrane ◽  
Chick Embryo Chorioallantoic Membrane

scholarly journals 3D chick embryo chorioallantoic membrane model as an in vivo model to study morphological and histopathological features of feline fibrosarcomas

2017 ◽  
Vol 13 (1) ◽  
Author(s):  
Katarzyna Zabielska-Koczywąs ◽  
Agata Wojtkowska ◽  
Izabella Dolka ◽  
Anna Małek ◽  
Magdalena Walewska ◽  
...  
Keyword(s):  
Chick Embryo ◽  
Chorioallantoic Membrane ◽  
Membrane Model ◽  
In Vivo Model ◽  
Histopathological Features ◽  
Chick Embryo Chorioallantoic Membrane

scholarly journals STUDIES ON HOST-VIRUS INTERACTIONS IN THE CHICK EMBRYO-INFLUENZA VIRUS SYSTEM

1949 ◽  
Vol 90 (1) ◽  
pp. 13-22 ◽  
Author(s):  
Werner Henle
Keyword(s):  
Influenza Virus ◽  
Chick Embryo ◽  
Active Agent ◽  
Allantoic Fluid ◽  
Inhibitory Effect ◽  
Influenza Viruses ◽  
Host Cells ◽  
Active Virus ◽  
Homologous Virus ◽  
Host Virus Interactions

Experiments have been reported on the propagation of influenza viruses in the allantoic membrane of the developing chick embryo during the first infectious cycle. After adsorption of the seed virus onto the host cells, only a small percentage of it remains demonstrable by infectivity titrations. This amount remains constant for 4 hours in the case of infection with PR8 virus, and for 6 hours in that of infection with Lee virus. Thereafter, a sharp rise in infectivity occurs 2 to 3 hours before liberation of the new generations of active virus into the allantoic fluid can be detected. Injection of homologous virus, inactivated by ultraviolet irradiation, following infection prevents or delays the production of virus in the tissues, depending to some extent upon the number of ID50 of active virus used as inoculum. The smaller the dose, the more pronounced the inhibitory effect. With increasing delay in the injection of the inhibitor, progressively more virus is produced and liberated 6 and 9 hours after infection with PR8 and Lee virus, respectively. Thus, production of virus may be interrupted by the homologous inhibitor when given up to 3 hours after infection with PR8, and up to4½ hours after infection with Lee virus. Since no increase in infectivity can bedetected during these 3 and 4½ hour periods in the tissues, it is suggested that influenza virus propagates in at least two major stages: first, non-infectious, immature virus material is produced which, subsequently, is converted into the fully active agent. Presumably the first step can be interrupted by the homologous inhibitor, while the second cannot. Heterologous irradiated virus, injected after infection of the tissue, exerts only a slight inhibitory effect on the production of virus.

scholarly journals Effects of hypoxic preconditioning on neuroblastoma tumour oxygenation and metabolic signature in a chick embryo model

2018 ◽  
Vol 38 (4) ◽  
Author(s):  
Yousef K. Al-Mutawa ◽  
Anne Herrmann ◽  
Catriona Corbishley ◽  
Paul D. Losty ◽  
Marie Phelan ◽  
...  
Keyword(s):  
Chick Embryo ◽  
Neuroblastoma Cell ◽  
Neuroblastoma Cells ◽  
Chorioallantoic Membrane ◽  
Hypoxic Preconditioning ◽  
Oxygen Levels ◽  
Tumour Oxygenation ◽  
Chick Embryo Model

Hypoxia episodes and areas in tumours have been associated with metastatic dissemination and poor prognosis. Given the link between tumour tissue oxygen levels and cellular metabolic activity, we hypothesised that the metabolic profile between metastatic and non-metastatic tumours would reveal potential new biomarkers and signalling cues. We have used a previously established chick embryo model for neuroblastoma growth and metastasis, where the metastatic phenotype can be controlled by neuroblastoma cell hypoxic preconditioning (3 days at 1% O2). We measured, with fibre-optic oxygen sensors, the effects of the hypoxic preconditioning on the tumour oxygenation, within tumours formed by SK-N-AS cells on the chorioallantoic membrane (CAM) of chick embryos. We found that the difference between the metastatic and non-metastatic intratumoural oxygen levels was small (0.35% O2), with a mean below 1.5% O2 for most tumours. The metabolomic profiling, using NMR spectroscopy, of neuroblastoma cells cultured in normoxia or hypoxia for 3 days, and of the tumours formed by these cells showed that the effects of hypoxia in vitro did not compare with in vivo tumours. One notable difference was the high levels of the glycolytic end-products triggered by hypoxia in vitro, but not by hypoxia preconditioning in tumours, likely due to the very high basal levels of these metabolites in tumours compared with cells. In conclusion, we have identified high levels of ketones (3-hydroxybutyrate), lactate and phosphocholine in hypoxic preconditioned tumours, all known to fuel tumour growth, and we herein point to the poor relevance of in vitro metabolomic experiments for cancer research.

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