Influenza virus-induced changes in rabbit sleep and acute phase responses

1992 ◽  
Vol 263 (5) ◽  
pp. R1115-R1121 ◽  
Author(s):  
M. Kimura-Takeuchi ◽  
J. A. Majde ◽  
L. A. Toth ◽  
J. M. Krueger
Keyword(s):  
Influenza Virus ◽  
Antiviral Activity ◽  
Acute Phase ◽  
Acute Phase Response ◽  
Defense Mechanisms ◽  
Brain Temperature ◽  
Allantoic Fluid ◽  
Serum Levels ◽  
Phase Response ◽  
Serum Ceruloplasmin

Systematic investigations of sleep after viral inoculation have not previously been described. In the present study, rabbits were inoculated intravenously (iv) with control allantoic fluid followed by two sequential inoculations of influenza virus at intervals of 24 h. After each i.v. inoculation, sleep and brain temperature (Tbr), as well as leukocyte distributions and serum levels of antiviral activity and ceruloplasmin, were monitored. The first viral inoculation elicited several acute phase responses, including increased non-rapid-eye-movement sleep (NREMS), Tbr, serum antiviral activity, and serum ceruloplasmin levels, as well as neutrophilia and lymphopenia. In contrast to the effects of the first inoculation, after the second inoculation of virus, all these acute phase parameters were diminished or absent (the hyporesponsive state). Inoculation of naive rabbits with heat-inactivated virus was similarly ineffective; however, inoculation of this group of rabbits with viable virus 24 h later did induce full-scale acute phase responses. The possible role of cytokines in mediating the acute phase response after influenza viral challenge is discussed. Results support the hypothesis that sleep is a facet of the acute phase response involved in host defense mechanisms.

Transient decreased retinol serum levels in children with pneumonia and acute phase response

2011 ◽  
Author(s):  
Kellen C. K. Barbosa ◽  
Daniel F. Cunha ◽  
Alceu A. Jordão Jr. ◽  
Virgínia R. S. Weffort ◽  
Selma F. C. Cunha
Keyword(s):  
Acute Phase ◽  
Acute Phase Response ◽  
Serum Levels ◽  
Phase Response

Acute phase response after myocardial infarction: Correlation between serum levels of cytokines and C-reactive protein

1990 ◽  
Vol 68 (21) ◽  
pp. 1083-1083 ◽  
Author(s):  
H. Tilg ◽  
J. Mair ◽  
M. Herold ◽  
W. E. Aulitzky ◽  
P. Lechleitner ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Phase ◽  
Acute Phase Response ◽  
Serum Levels ◽  
Phase Response ◽  
C Reactive Protein ◽  
Reactive Protein

Evidence that brief stress may induce the acute phase response in rats

1997 ◽  
Vol 273 (6) ◽  
pp. R1998-R2004 ◽  
Author(s):  
Terrence Deak ◽  
Jennifer L. Meriwether ◽  
Monika Fleshner ◽  
Robert L. Spencer ◽  
Amer Abouhamze ◽  
...  
Keyword(s):  
Body Temperature ◽  
Acute Phase ◽  
Acute Phase Response ◽  
Core Body Temperature ◽  
Serum Levels ◽  
Phase Response ◽  
Single Session ◽  
Acid Glycoprotein ◽  
Corticosteroid Binding Globulin ◽  
Core Body

Exposing rats to a single session of inescapable tail shock (IS) reduces corticosteroid binding globulin (CBG) 24 h later (Fleshner et al., Endocrinology 136: 5336–5342, 1995). The present experiments examined whether reductions in CBG are differentially affected by controllable vs. identical uncontrollable tail shock, are mediated by IS-induced glucocorticoid elevation, or reflect IS-induced activation of the acute phase response and whether IS produces fever. The results demonstrate that 1) equivalent reductions in CBG are observed in response to escapable tail shock or yoked IS, 2) IS-induced CBG reduction is not blocked by adrenalectomy in rats that receive basal corticosteroid replacement or by pretreatment with RU-38486, and 3) IS appears to activate the acute phase response, since IS reduces serum levels of an acute-phase negative reactant (CBG), increases serum levels of acute-phase positive reactants (haptoglobin and α1-acid glycoprotein), and increases core body temperature 20–24 h later.

The relationship between serum levels of lipoprotein(a) and proteins associated with the acute phase response

1993 ◽  
Vol 223 (1-2) ◽  
pp. 73-82 ◽  
Author(s):  
Thomas B. Ledue ◽  
Louis M. Neveux ◽  
Glenn E. Palomaki ◽  
Robert F. Ritchie ◽  
Wendy Y. Craig
Keyword(s):  
Acute Phase ◽  
Acute Phase Response ◽  
Serum Levels ◽  
Phase Response ◽  
Lipoprotein A ◽  
The Relationship

Association Between Stent Implantation and Progression of Nontarget Lesions in a Rabbit Model of Atherosclerosis

2021 ◽  
Author(s):  
Jing Ma ◽  
Xiaoling Liu ◽  
Lei Qiao ◽  
Linlin Meng ◽  
Xingli Xu ◽  
...  
Keyword(s):  
Protein Expression ◽  
Acute Phase ◽  
Systemic Inflammation ◽  
Stent Implantation ◽  
Acute Phase Response ◽  
Rabbit Model ◽  
Serum Levels ◽  
Phase Response ◽  
Plaque Burden ◽  
Amyloid A

Background: Progression of nontarget lesions (NTLs) after percutaneous coronary intervention (PCI) has been reported. However, it remains unknown whether progression of NTLs was causally related to stenting. This study was undertaken to test the hypothesis that stent implantation triggers acute phase response and systemic inflammation which may be associated with progression of NTLs. Methods: Thirty New Zealand rabbits receiving endothelial denudation and atherogenic diet were randomly divided into stenting, sham, and control groups. Angiography and intravascular ultrasonography were performed in the stenting and sham groups, and stent implantation performed only in the stenting group. Histopathologic study was conducted and serum levels of APPs (acute phase proteins) measured in all rabbits. Proteomics analysis was performed to screen the potential proteins related to NTLs progression after stent implantation. The serum levels of APPs and inflammatory cytokines were measured in 147 patients undergoing coronary angiography or PCI. Results: Plaque burden in the NTLs was significantly increased 12 weeks after stent implantation in the stenting group versus sham group. Serum levels of APPs and their protein expression in NTLs were significantly increased and responsible for stenting-triggered inflammation. In patients receiving PCI, serum levels of SAA-1 (serum amyloid A protein 1), CRP (C-reactive protein), TNF (tumor necrosis factor)-α, and IL (interleukin)-6 were substantially elevated up to 1 month post-PCI. Conclusions: In a rabbit model of atherosclerosis, stent implantation triggered acute phase response and systemic inflammation, which was associated with increased plaque burden and pathological features of unstable plaque in NTLs. The potential mechanism involved vessel injury-triggered acute phase response manifested as increased serum levels of SAA-1, CRP, and LBP (lipopolysaccharide-binding protein) and their protein expression in NTLs. These findings provided a new insight into the relation between stent implantation and progression of NTLs, and further studies are warranted to clarify the detailed mechanism and clinical significance of these preliminary results. REGISTRATION: URL: http://www.chictr.org.cn ; Unique identifier: ChiCTR1900026393.

Glycoprotein biosynthesis during the acute-phase response to inflammation

1983 ◽  
Vol 61 (9) ◽  
pp. 1041-1048 ◽  
Author(s):  
J. C. Jamieson ◽  
H. A. Kaplan ◽  
B. M. R. N. J. Woloski ◽  
M. Hellman ◽  
K. Ham
Keyword(s):  
Acute Phase ◽  
Acute Phase Response ◽  
Elevated Serum ◽  
Serum Cortisol ◽  
Serum Levels ◽  
Acute Phase Reactant ◽  
Phase Response ◽  
Acute Phase Reactants ◽  
Acid Glycoprotein ◽  
Phase Reactant

Inflammation results in an increase in the levels of a variety of glycoproteins in serum. The glycoproteins that respond in this way are usually referred to as acute-phase reactants. Studies on the acute-phase response of rat α1-acid glycoprotein showed that there was an increase in the liver levels of this glycoprotein at 12 h after turpentine inflammation. This was followed by increased serum levels at 48–72 h after inflammation, suggesting a precursor–product relationship between liver and serum α1-acid glycoprotein. Incorporation studies coupled with measurements of synthesis rates of α1-acid glycoprotein showed that increased synthesis was responsible for the acute-phase response of this protein to inflammation. These studies also showed that albumin was a negative acute-phase reactant. The acute-phase response of α1-acid glycoprotein was accompanied by increased liver pools of UDP–N-acetylglucosamine (UDP–GlcNAc) and UDP–N-acetylgalactosamine (UDP–GalNAc) and increased liver activities of glucosamine-6-phosphate synthase and UDP–GlcNAc 2-epimerase. Activities of galactosyl and sialyl transferases in liver were also elevated and serum sialyl transferase was increased substantially in inflammation, suggesting that it may also be an acute-phase reactant. Liver activities of β-N-acetylhexosaminidase and β-galactosidase declined by about 50% at 24 h after inflammation; there was evidence that serum levels of these enzymes increased at 24–72 h after inflammation, suggesting that the lysosomal glycosidases may be released from liver during inflammation. Inflammation resulted in elevated serum Cortisol, insulin, and adrenocorticotropic hormone and induced increased glycogenosis; liver cAMP levels were also increased during inflammation. Preliminary studies are presented to show that leukocyte-derived factors may be involved in the acute-phase response of α1-acid glycoprotein to inflammation.

Cytokines and the acute phase response to influenza virus in mice

1995 ◽  
Vol 268 (1) ◽  
pp. R78-R84 ◽  
Author(s):  
C. A. Conn ◽  
J. L. McClellan ◽  
H. F. Maassab ◽  
C. W. Smitka ◽  
J. A. Majde ◽  
...  
Keyword(s):  
Influenza Virus ◽  
Locomotor Activity ◽  
Acute Phase ◽  
Water Intake ◽  
Acute Phase Response ◽  
Lavage Fluid ◽  
Lung Lavage ◽  
Phase Response ◽  
Necrosis Factor Alpha ◽  
Food And Water Intake

This study characterized selected aspects of the acute phase response after intranasal inoculation of mice with two doses of mouse-adapted influenza virus differing in lethality. Mice given 140 plaque-forming units (PFU) of virus (58% survival) gradually decreased food and water intake to nearly zero over 6 days; survivors then slowly increased intakes. Declines in these behaviors were parallel to decreases in body temperature and general locomotor activity and were associated with elevated activities of interleukin-6 (IL-6), tumor necrosis factor-alpha, and interferons in lung lavage fluid. Circulating levels of these cytokines were not increased. After 55,000 PFU of virus (100% mortality), food and water intake fell to near zero within 48 h, temperature and locomotor activity decreased significantly, and activities of IL-1 and IL-6 were elevated in lung lavage fluid. These data show that cytokine activities in the lungs are elevated in a time frame that supports the hypothesis that cytokines could mediate behavioral and physiological changes in mice during acute influenza infections.

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