scholarly journals In situ histochemical localization of type I interleukin-1 receptor messenger RNA in the central nervous system, pituitary, and adrenal gland of the mouse

1992 ◽  
Vol 12 (3) ◽  
pp. 1101-1114 ◽  
Author(s):  
ET Cunningham ◽  
E Wada ◽  
DB Carter ◽  
DE Tracey ◽  
JF Battey ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Adrenal Gland ◽  
Messenger Rna ◽  
Interleukin 1 ◽  
Histochemical Localization ◽  
Type I ◽  
The Central Nervous System

scholarly journals Induction of interleukin-1 in glia, and its significance in the central nervous system.

1994 ◽  
Vol 64 ◽  
pp. 59
Author(s):  
Yasuko Tomozawa ◽  
Masabumi Minami ◽  
Kazuki Yabuuchi ◽  
Masamichi Satoh
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Interleukin 1 ◽  
The Central Nervous System

Effect of a central CRF antagonist on cardiovascular and thermoregulatory responses induced by stress or IL-1 beta

1993 ◽  
Vol 265 (4) ◽  
pp. R834-R839 ◽  
Author(s):  
T. Nakamori ◽  
A. Morimoto ◽  
N. Murakami
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Interleukin 1 ◽  
Corticotropin Releasing Factor ◽  
Mild Stress ◽  
Induced Responses ◽  
Interleukin 1 Beta ◽  
The Central Nervous System ◽  
Beta 2

We investigated the role of central corticotropin-releasing factor (CRF) in the development of cardiovascular and thermal responses induced by stress or by interleukin-1 beta (IL-1 beta) in free-moving rats. Intracerebroventricular (icv) injection of alpha-helical CRF9-41 (10 micrograms), a CRF receptor antagonist, significantly attenuated hypertension, tachycardia, and a rise in body temperature induced by cage-switch stress, a mild stress. However, icv injection of alpha-helical CRF9-41 (10 micrograms) had no effect on hypertension, tachycardia, or fever induced by intraperitoneal (ip) injection of IL-1 beta (2 micrograms/kg) or icv prostaglandin E2 (PGE2, 100 ng). In contrast, icv injection of alpha-helical CRF9-41 (10 micrograms) significantly attenuated hypertension, tachycardia, or fever induced by icv injection of IL-1 beta (20 ng). The present results suggest that central CRF has an important role in the development of the cage-switch stress-induced responses, but it does not seem to contribute to the hypertension, tachycardia, and fever induced by ip IL-1 beta or by central PGE2. However, it is possible that when IL-1 beta directly acts on the central nervous system, some of its actions are mediated by central CRF.

Interleukin-1 and interleukin-6 modify protein phosphorylation in the central nervous system ofHirudo medicinalis

1994 ◽  
Vol 641 (1) ◽  
pp. 155-159 ◽  
Author(s):  
Daniele Bottai ◽  
Mercedes Garcia-Gil ◽  
Maria Luisa Zaccardi ◽  
Loredana Fineschi ◽  
Marcello Brunelli
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Protein Phosphorylation ◽  
Interleukin 6 ◽  
Interleukin 1 ◽  
The Central Nervous System ◽  
Modify Protein

scholarly journals Differential Effects of Three CanonicalToxoplasmaStrains on Gene Expression in Human Neuroepithelial Cells

2010 ◽  
Vol 79 (3) ◽  
pp. 1363-1373 ◽  
Author(s):  
Jianchun Xiao ◽  
Lorraine Jones-Brando ◽  
C. Conover Talbot ◽  
Robert H. Yolken
Keyword(s):  
Gene Expression ◽  
Central Nervous System ◽  
Nervous System ◽  
Nucleotide Metabolism ◽  
Neural Cells ◽  
Type I ◽  
Type Ii ◽  
Type Iii ◽  
Neuroepithelial Cells ◽  
The Central Nervous System

ABSTRACTStrain type is one of the key factors suspected to play a role in determining the outcome ofToxoplasmainfection. In this study, we examined the transcriptional profile of human neuroepithelioma cells in response to representative strains ofToxoplasmaby using microarray analysis to characterize the strain-specific host cell response. The study of neural cells is of interest in light of the ability ofToxoplasmato infect the brain and to establish persistent infection within the central nervous system. We found that the extents of the expression changes varied considerably among the three strains. Neuroepithelial cells infected withToxoplasmatype I exhibited the highest level of differential gene expression, whereas type II-infected cells had a substantially smaller number of genes which were differentially expressed. Cells infected with type III exhibited intermediate effects on gene expression. The three strains also differed in the individual genes and gene pathways which were altered following cellular infection. For example, gene ontology (GO) analysis indicated that type I infection largely affects genes related to the central nervous system, while type III infection largely alters genes which affect nucleotide metabolism; type II infection does not alter the expression of a clearly defined set of genes. Moreover, Ingenuity Pathways Analysis (IPA) suggests that the three lineages differ in the ability to manipulate their host; e.g., they employ different strategies to avoid, deflect, or subvert host defense mechanisms. These observed differences may explain some of the variation in the neurobiological effects of different strains ofToxoplasmaon infected individuals.

Sign in / Sign up

Export Citation Format

Share Document