Evidence for a novel, local acute-phase response in the bovine oviduct: Progesterone and lipopolysaccharide up-regulate alpha 1-acid-glycoprotein expression in epithelial cells in vitro

2014 ◽  
Vol 81 (9) ◽  
pp. 861-870 ◽  
Author(s):  
R. Kowsar ◽  
N. Hambruch ◽  
M.A. Marey ◽  
J. Liu ◽  
T. Shimizu ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Acute Phase ◽  
Acute Phase Response ◽  
Phase Response ◽  
Acid Glycoprotein

In vitro release of ?1-acid glycoprotein RNA sequences shows fidelity with the acute phase response in vivo

1986 ◽  
Vol 11 (3) ◽  
pp. 163-172 ◽  
Author(s):  
G. A. Clawson ◽  
J. Button ◽  
C. H. Woo ◽  
Yu-Cheng Liao ◽  
E. A. Smuckler
Keyword(s):  
Acute Phase ◽  
Acute Phase Response ◽  
In Vitro Release ◽  
Phase Response ◽  
Rna Sequences ◽  
Acid Glycoprotein ◽  
Vitro Release

Regulation of the acute phase response genes alpha1-acid glycoprotein and alpha1-antitrypsin correlates with sensitivity to thermal injury

Surgery ◽  
1996 ◽  
Vol 119 (6) ◽  
pp. 664-673 ◽  
Author(s):  
David A. Gilpin ◽  
Ching-Chyuan Hsieh ◽  
David T. Kuninger ◽  
David N. Herndon ◽  
John Papaconstantinou
Keyword(s):  
Acute Phase ◽  
Acute Phase Response ◽  
Thermal Injury ◽  
Phase Response ◽  
Acid Glycoprotein ◽  
Alpha1 Antitrypsin

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.

scholarly journals Epigenetic Modulation by Apabetalone Counters Cytokine-Driven Acute Phase Response In Vitro, in Mice and in Patients with Cardiovascular Disease

2020 ◽  
Vol 2020 ◽  
pp. 1-12
Author(s):  
Sylwia Wasiak ◽  
Dean Gilham ◽  
Emily Daze ◽  
Laura M. Tsujikawa ◽  
Christopher Halliday ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Acute Phase ◽  
Acute Phase Response ◽  
Phase Response ◽  
Serum Amyloid ◽  
Cytokine Signaling ◽  
Serum Amyloid P ◽  
Gene And Protein Expression ◽  
Amyloid P

Chronic systemic inflammation contributes to cardiovascular disease (CVD) and correlates with the abundance of acute phase response (APR) proteins in the liver and plasma. Bromodomain and extraterminal (BET) proteins are epigenetic readers that regulate inflammatory gene transcription. We show that BET inhibition by the small molecule apabetalone reduces APR gene and protein expression in human hepatocytes, mouse models, and plasma from CVD patients. Steady-state expression of serum amyloid P, plasminogen activator inhibitor 1, and ceruloplasmin, APR proteins linked to CVD risk, is reduced by apabetalone in cultured hepatocytes and in humanized mouse liver. In cytokine-stimulated hepatocytes, apabetalone reduces the expression of C-reactive protein (CRP), alpha-2-macroglobulin, and serum amyloid P. The latter two are also reduced by apabetalone in the liver of endotoxemic mice. BET knockdown in vitro also counters cytokine-mediated induction of the CRP gene. Mechanistically, apabetalone reduces the cytokine-driven increase in BRD4 BET occupancy at the CRP promoter, confirming that transcription of CRP is BET-dependent. In patients with stable coronary disease, plasma APR proteins CRP, IL-1 receptor antagonist, and fibrinogen γ decrease after apabetalone treatment versus placebo, resulting in a predicted downregulation of the APR pathway and cytokine targets. We conclude that CRP and components of the APR pathway are regulated by BET proteins and that apabetalone counters chronic cytokine signaling in patients.

Endotoxin-stimulated production of rat hypothalamic interleukin-1β in vivo and in vitro, measured by specific immunoradiometric assay

1993 ◽  
Vol 11 (1) ◽  
pp. 31-36 ◽  
Author(s):  
P Hagan ◽  
S Poole ◽  
A F Bristow
Keyword(s):  
Acute Phase ◽  
Acute Phase Response ◽  
Interleukin 1 ◽  
Phase Response ◽  
Inflammatory Stimuli ◽  
Quantitative Immunoassay ◽  
Time Courses ◽  
A Site

ABSTRACT Regulation of a number of aspects of the acute-phase response, including induction of fever and activation of the hypothalamo-pituitary-adrenal axis, occurs within the hypothalamus. The acute-phase response appears to be co-ordinated by the inflammatory cytokine interleukin-1 (IL-1). A number of studies using hybridization techniques to measure IL-1 gene expression and immunocyto-chemistry to localize immunoactive IL-1 have established the concept that the central nervous system, and in particular the hypothalamus, is a site of IL-1 production, and that levels increase in response to inflammatory stimuli. In this report we present data on the levels of IL-1β produced in the rat hypothalamus using quantitative immunoassay techniques. Bacterial endotoxin, administered to rats in vivo, evoked increases in hypothalamic IL-1β levels which were significant within 1 h, and reached maximum levels at 5–10 h. The response to endotoxin was dose-related, and levels reached in hypothalamic extracts corresponded to intra-hypothalamic levels of the order of 20 ng/ml. During short-term in-vitro culture of rat hypothalami, endotoxin stimulated a dose-related increase in both the synthesis and the secretion of IL-1β, which reached similar levels to those seen after in-vivo stimulation. Hypothalami obtained from animals stimulated with endotoxin in vivo did not, however, show any evidence of persistent stimulation of IL-1β production when subsequently cultured in vitro. These data support the concept that production of hypothalamic IL-1 is an essential step in regulating the activity of the hypothalamus during the acute-phase response, and provide for the first time quantitative data on the magnitude, dose—response relationships and time-courses of rat hypothalamic IL-1β production in vivo and in vitro.

scholarly journals Studies of translatable mRNA for rabbit C-reactive protein

1985 ◽  
Vol 227 (3) ◽  
pp. 759-765 ◽  
Author(s):  
D Samols ◽  
S S MacIntyre ◽  
I Kushner
Keyword(s):  
Acute Phase ◽  
Acute Phase Response ◽  
Phase Response ◽  
Translation Product ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Primary Translation Product ◽  
Free Translation ◽  
Translatable Mrna

C-reactive protein (CRP) mRNA was assayed by cell-free translation of poly(A)-containing liver RNA isolated both from rabbits stimulated to undergo the acute-phase response and from unstimulated control rabbits. No CRP-related translation products were identified until the denaturant methylmercury hydroxide (CH3HgOH) was added to the RNA before cell-free translation. In the presence of the denaturant, a 24000-Da translation product was synthesized which was immunochemically identifiable as the CRP primary translation product. It is likely that rabbit CRP mRNA can form a stable intramolecular duplex which interferes with its translatability in vitro. The 24000-Da CH3HgOH-facilitated cell-free translation product was not detected in poly(A)-containing liver RNA from unstimulated animals, indicating that the concentration of translatable CRP mRNA was dramatically induced during the acute-phase response. On the basis of absorption experiments, the 24000-Da CRP primary translation product was immunochemically more closely related to denatured CRP than to native CRP.

Chylomicron-bound LPS inhibits activation of the acute phase response in vitro and in vivo

2003 ◽  
Vol 114 (2) ◽  
pp. 303
Author(s):  
J.S. Chang ◽  
D.H. Lee ◽  
A.E. Falor ◽  
F. Kasravi ◽  
H.W. Harris
Keyword(s):  
Acute Phase ◽  
Acute Phase Response ◽  
Phase Response

scholarly journals Decreased expression levels of rat liver glutathione S-transferase A2 and albumin during the acute phase response are mediated by HNF1 (hepatic nuclear factor 1) and IL6DEX-NP

2004 ◽  
Vol 377 (3) ◽  
pp. 763-768 ◽  
Author(s):  
Richard WHALEN ◽  
Susan H. VOSS ◽  
Thomas D. BOYER
Keyword(s):  
Acute Phase ◽  
Acute Phase Response ◽  
Rat Hepatocytes ◽  
Phase Response ◽  
Negative Regulator ◽  
Nuclear Factor ◽  
Hepatic Nuclear Factor 1 ◽  
Nuclear Factor 1

The acute phase response is characterized by positive and negative regulation of many liver proteins including GSTs (glutathione S-transferases) and albumin. The expression of albumin and some GSTs are dependent on HNF1 (hepatic nuclear factor 1). Interleukin 6 plus dexamethasone induce a nuclear protein (IL6DEX-NP) in rat hepatocytes in vitro that binds to a promoter element adjacent to the HNF1 site of rGSTA2 and decreases its expression. We determined how HNF1 and IL6DEX-NP regulate rGSTA2 and albumin expression in rats during the acute phase response after LPS (lipopolysaccharide) treatment. Expression of rGSTA2 and albumin mRNA decreased 3 h after LPS treatment and remained low for 48 h. Transcription rates showed a similar pattern but albumin transcription was less affected. HNF1 and IL6DEX-NP binding to the rGSTA2 promoter was present in control livers but was absent at 3 and 6 h after LPS. By 12 h, HNF1 and IL6DEX-NP binding to the rGSTA2 promoter reappeared and increased to above normal at 48 h. The patterns of HNF1 and IL6DEX-NP binding to the albumin promoter were similar. Affinity of IL6DEX-NP for the albumin promoter was less than that for the rGSTA2 promoter and changes in the transcription rates were consistent with the difference. Early decreases in rGSTA2 and albumin during the acute phase response are due to decreased binding of HNF1. Later persistent decreases in transcriptional rate of rGSTA2 and to a lesser extent albumin are due to increased IL6DEX-NP binding. IL6DEX-NP appears to be an important negative regulator of gene expression in vitro and in vivo.

scholarly journals The influence of glucocorticoid on the fibrinogen messenger RNA content of rat liver in vivo and in hepatocyte suspension culture

1984 ◽  
Vol 220 (3) ◽  
pp. 631-637 ◽  
Author(s):  
H M G Princen ◽  
H J Moshage ◽  
H J W de Haard ◽  
P J van Gemert ◽  
S H Yap
Keyword(s):  
Acute Phase ◽  
Acute Phase Response ◽  
Messenger Rna ◽  
Acute Phase Proteins ◽  
Rat Hepatocytes ◽  
Phase Response ◽  
Control Value ◽  
Hepatocyte Suspension

The plasma concentration of fibrinogen, one of the major acute-phase proteins produced by the liver, increases during the acute-phase response as a result of enhanced synthesis in liver. Since adrenal-cortical hormones have been thought to have a key role in the regulation of the fibrinogen synthesis, fibrinogen-polypeptide mRNA sequences were determined in the present study, by using a specific complementary-DNA probe, in RNA fractions obtained from rat hepatocytes exposed to glucocorticoids in vitro (hepatocyte suspension cultures) and in vivo. Maximal induction of the fibrinogen-polypeptide mRNA (to 400% of the control value) was found in vitro at 0.1 microM-dexamethasone after 9 h of incubation. The same magnitude of induction was obtained with 20 microM-cortisol or 60 microM-corticosterone. In contrast with the findings in vitro, no induction of the fibrinogen-polypeptide mRNA was observed in the liver at various times after injection of different doses of glucocorticoids into rats. These results suggest that more complex regulatory mechanisms are involved and that glucocorticoids are not the sole regulatory factors in vivo in the enhanced synthesis of fibrinogen during the acute-phase response.

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