Interleukin-1 beta release from rat gastric fundus

1996 ◽  
Vol 271 (2) ◽  
pp. G275-G281 ◽  
Author(s):  
P. Montuschi ◽  
G. Tringali ◽  
A. Mirtella ◽  
L. Parente ◽  
E. Ragazzoni ◽  
...  
Keyword(s):  
Acid Secretion ◽  
Ex Vivo ◽  
Interleukin 1 ◽  
Gastric Fundus ◽  
Interleukin 1 Beta ◽  
Rat Gastric Fundus ◽  
Hypothalamic Level ◽  
Stimulation Of

Interleukin-1 (IL-1) is known to regulate gastric functions via a central action at the hypothalamic level, and it has also been shown that this cytokine can directly modulate rat gastric motility. This study was conducted to determine whether IL-1 beta is produced and released by rat gastric fundi in vitro. IL-1 beta immunoreactivity was released in measurable amounts from explanted rat gastric tissue. This release was not affected by electrical stimulation of the gastric strips or by agents that induce IL-1 biosynthesis. It could be inhibited only by the glucocorticoid dexamethasone. Ex vivo experiments confirmed the inhibitory role of glucocorticoids and showed that IL-1 beta release can be inhibited by agents that reduce gastric acid secretion, suggesting that the latter might stimulate IL-1 beta synthesis and release. In light of the well-established gastroprotection exerted by IL-1, H(+)-induced IL-1 beta release might serve as a protection against mucosal injuries caused by acid secretion, and the inhibition of this release by glucocorticoids might be involved in the pathogenesis of gastric damage associated with severe stress or steroid therapy.

Defective interleukin-1-induced ACTH release in cholestatic rats: impaired hypothalamic PGE2 release

1995 ◽  
Vol 268 (3) ◽  
pp. G404-G409 ◽  
Author(s):  
M. G. Swain ◽  
M. Maric ◽  
L. Carter
Keyword(s):  
Bile Duct ◽  
Hpa Axis ◽  
Interleukin 1 ◽  
Proinflammatory Mediators ◽  
Significant Attenuation ◽  
Regulatory Loop ◽  
Hypothalamic Level ◽  
Acth Release

A complete regulatory loop exists between the immune and neuroendocrine systems. Proinflammatory mediators such as endotoxin (lipopolysaccharide) and interleukin-1 (IL-1) are capable of activating the hypothalamic-pituitary-adrenal (HPA) axis at the hypothalamic level, presumably by inducing the synthesis of prostaglandins. We have recently identified abnormalities in the stress-induced activation of the HPA axis in cholestatic rats. Therefore, in rats with cholestasis due to bile duct resection and sham-resected controls, we studied alterations in proinflammatory mediator-induced activation of the HPA axis and documented the role of alterations in hypothalamic prostaglandin synthesis in these abnormalities. Systemic administration of endotoxin and IL-1 resulted in a significant attenuation of adrenocorticotropic hormone (ACTH) release into plasma in bile duct-resected compared with sham-resected animals. This suppression of endotoxin- or IL-1-induced ACTH release in bile duct-resected rats was associated with a complete absence of IL-1-induced hypothalamic release of prostaglandin E2 (PGE2) in vitro in these animals. In contrast, sham-resected rats exhibited a 70% increase in hypothalamic PGE2 secretion in vitro in response to IL-1. However, bile duct-resected rats exhibited HPA axis activation similar to that of sham-resected animals in response to intracerebroventricularly infused PGE2. Therefore, cholestasis in the rat is associated with an attenuation of central activation of the HPA axis by proinflammatory mediators that appears to be mediated, at least in part, by defective IL-1-induced hypothalamic prostaglandin production.

scholarly journals The role of icIL-1RA in keratinocyte senescence and development of the senescence-associated secretory phenotype

2021 ◽  
Vol 134 (4) ◽  
pp. jcs252080
Author(s):  
Sven E. Niklander ◽  
Hannah L. Crane ◽  
Lav Darda ◽  
Daniel W. Lambert ◽  
Keith D. Hunter
Keyword(s):  
Ex Vivo ◽  
Interleukin 1 ◽  
Oral Keratinocytes ◽  
Cytokine Network ◽  
Inflammatory State ◽  
Important Regulator ◽  
Secretory Phenotype

ABSTRACTThere is compelling evidence that senescent cells, through the senescence-associated secretory phenotype (SASP), can promote malignant transformation and invasion. Interleukin-1 (IL-1) is a key mediator of this cytokine network, but the control of its activity in the senescence programme has not been elucidated. IL-1 signalling is regulated by IL-1RA, which has four variants. Here, we show that expression of intracellular IL-1RA type 1 (icIL-1RA1), which competitively inhibits binding of IL-1 to its receptor, is progressively lost during oral carcinogenesis ex vivo and that the pattern of expression is associated with keratinocyte replicative fate in vitro. We demonstrate that icIL-1RA1 is an important regulator of the SASP in mortal cells, as CRISPR/Cas9-mediated icIL-1RA1 knockdown in normal and mortal dysplastic oral keratinocytes is followed by increased IL-6 and IL-8 secretion, and rapid senescence following release from RhoA-activated kinase inhibition. Thus, we suggest that downregulation of icIL-1RA1 in early stages of the carcinogenesis process can enable the development of a premature and deregulated SASP, creating a pro-inflammatory state in which cancer is more likely to arise.

Chronic stimulation of the pituitary-adrenal axis in rats by interleukin-1 beta infusion: in vivo and in vitro studies.

Endocrinology ◽  
1992 ◽  
Vol 130 (3) ◽  
pp. 1153-1164
Author(s):  
C G Sweep ◽  
M J van der Meer ◽  
A R Hermus ◽  
A G Smals ◽  
J W van der Meer ◽  
...  
Keyword(s):  
Interleukin 1 ◽  
In Vitro Studies ◽  
Interleukin 1 Beta ◽  
Chronic Stimulation ◽  
Adrenal Axis ◽  
Pituitary Adrenal Axis ◽  
Stimulation Of

Interleukin-1 receptor antagonist displays intrinsic agonist activity on rat gastric fundus motility in vitro

1995 ◽  
Vol 275 (1) ◽  
pp. 31-37 ◽  
Author(s):  
Paolo Montuschi ◽  
Giuseppe Tringali ◽  
Adriana Mirtella ◽  
Luca Parente ◽  
Paolo Preziosi ◽  
...  
Keyword(s):  
Receptor Antagonist ◽  
Interleukin 1 ◽  
Gastric Fundus ◽  
Agonist Activity ◽  
Interleukin 1 Receptor Antagonist ◽  
Rat Gastric Fundus

scholarly journals Reduced NLRP3 Gene Expression Limits the IL-1β Cleavage via Inflammasome in Monocytes from Severely Injured Trauma Patients

2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
Shinwan Kany ◽  
Johann-Philipp Horstmann ◽  
Ramona Sturm ◽  
Katharina Mörs ◽  
Borna Relja
Keyword(s):  
Gene Expression ◽  
Nlrp3 Inflammasome ◽  
Ex Vivo ◽  
Traumatic Injury ◽  
Host Immunity ◽  
Trauma Patients ◽  
Nlrp3 Gene ◽  
Stimulation Of

Objective. Traumatic injury or severe surgery leads to a profound immune response with a diminished functionality of monocytes and subsequently their IL-1β release. IL-1β plays an important role in host immunity and protection against infections. Its biological activation via IL-1β-precursor processing requires the transcription of inflammasome components and their activation. Deregulated activity of NOD-like receptor inflammasomes (NLR) like NLRP3 that leads to the maturation of IL-1β has been described in various diseases. While the role of other inflammasomes has been studied in monocytes, nothing is known about NLRP3 inflammasome after a traumatic injury. Here, the role of the NLRP3 inflammasome in impaired monocyte functionality after a traumatic injury was analyzed. Measurements and Main Results. Ex vivo-in vitro stimulation of isolated CD14+ monocytes with lipopolysaccharide (LPS) showed a significantly higher IL-1β secretion in healthy volunteers (HV) compared to trauma patients (TP) after admission. Reduced IL-1β secretion was paralleled by significantly lowered gene expression of NLRP3 in monocytes from TP compared to those of HV. Transfection of monocytes with NLRP3-encoding plasmid recovered the functionality of monocytes from TP regarding the IL-1β secretion. Conclusions. This study demonstrates that CD14+ monocytes from TP are significantly diminished in their function and that the presence of NLRP3 components is necessary in recovering the ability of monocytes to produce active IL-1β. This recovery of the NLRP3 inflammasome in monocytes may imply a new target for treatment and therapy of immune suppression after severe injury.

The Role of Polyphenols in the Modulation of Plasma Non-Enzymatic Antioxidant Capacity (NEAC)

2012 ◽  
Vol 82 (3) ◽  
pp. 228-232 ◽  
Author(s):  
Mauro Serafini ◽  
Giuseppa Morabito
Keyword(s):  
Antioxidant Capacity ◽  
Dietary Intervention ◽  
Ex Vivo ◽  
The Body ◽  
Dietary Polyphenols ◽  
Enzymatic Antioxidant ◽  
Endogenous Antioxidant

Dietary polyphenols have been shown to scavenge free radicals, modulating cellular redox transcription factors in different in vitro and ex vivo models. Dietary intervention studies have shown that consumption of plant foods modulates plasma Non-Enzymatic Antioxidant Capacity (NEAC), a biomarker of the endogenous antioxidant network, in human subjects. However, the identification of the molecules responsible for this effect are yet to be obtained and evidences of an antioxidant in vivo action of polyphenols are conflicting. There is a clear discrepancy between polyphenols (PP) concentration in body fluids and the extent of increase of plasma NEAC. The low degree of absorption and the extensive metabolism of PP within the body have raised questions about their contribution to the endogenous antioxidant network. This work will discuss the role of polyphenols from galenic preparation, food extracts, and selected dietary sources as modulators of plasma NEAC in humans.

Early Platelet-Collagen Interactions in Whole Blood and Their Modifications by Aspirin and Dipyridamole Evaluated by a New Method (Basic Wave)

1985 ◽  
Vol 54 (04) ◽  
pp. 799-803 ◽  
Author(s):  
José Luís Pérez-Requejo ◽  
Justo Aznar ◽  
M Teresa Santos ◽  
Juana Vallés
Keyword(s):  
Whole Blood ◽  
Ex Vivo ◽  
Platelet Rich Plasma ◽  
White Blood Cells ◽  
Reversible Aggregation ◽  
Inhibitory Compounds ◽  
Rapid Generation ◽  
Stimulation Of ◽  
Collagen Stimulation

SummaryIt is shown that the supernatant of unstirred whole blood at 37° C, stimulated by 1 μg/ml of collagen for 10 sec, produces a rapid generation of pro and antiaggregatory compounds with a final proaggregatory activity which can be detected for more than 60 min on a platelet rich plasma (PRP) by turbidometric aggregometry. A reversible aggregation wave that we have called BASIC wave (for Blood Aggregation Stimulatory and Inhibitory Compounds) is recorded. The collagen stimulation of unstirred PRP produces a similar but smaller BASIC wave. BASIC’s intensity increases if erythrocytes are added to PRP but decreases if white blood cells are added instead. Aspirin abolishes “ex vivo” the ability of whole blood and PRP to generate BASIC waves and dipyridamole “in vitro” significantly reduces BASIC’s intensity in whole blood in every tested sample, but shows little effect in PRP.

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