Effects of silica exposure on the cardiac and renal inflammatory and fibrotic response and the antagonistic role of interleukin-1 beta in C57BL/6 mice

2014 ◽  
Vol 90 (2) ◽  
pp. 247-258 ◽  
Author(s):  
Jiali Guo ◽  
Tingming Shi ◽  
Xiuqing Cui ◽  
Yi Rong ◽  
Ting Zhou ◽  
...  
Keyword(s):  
Interleukin 1 ◽  
Interleukin 1 Beta ◽  
Fibrotic Response ◽  
Silica Exposure

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.

Corticosterone regulates behavioral effects of lipopolysaccharide and interleukin-1 beta in mice

1995 ◽  
Vol 269 (1) ◽  
pp. R154-R159 ◽  
Author(s):  
E. Goujon ◽  
P. Parnet ◽  
A. Aubert ◽  
G. Goodall ◽  
R. Dantzer
Keyword(s):  
Interleukin 1 ◽  
Behavioral Effects ◽  
Protective Effects ◽  
Interleukin 1 Beta ◽  
Social Exploration ◽  
Inhibitory Feedback ◽  
Adrenal Response ◽  
Acute Injection ◽  
Progesterone Antagonist

The modulatory role of endogenous corticoids in the behavioral effects of lipopolysaccharide (LPS) and recombinant human interleukin-1 beta (IL-1 beta) was studied in mice. Adrenalectomy enhanced the depression of social exploration induced by subcutaneous injection of 200 ng of IL-1 beta or 2 micrograms of LPS. This effect was mimicked by an acute injection of the progesterone antagonist RU-38486 (0.25-1 mg). Chronic replacement with a 15-mg corticosterone pellet abrogated the enhanced susceptibility of adrenalectomized animals to 200 ng of IL-1 beta but had only partial protective effects on their response to 400 ng of IL-1 beta and LPS. These results suggest that the pituitary-adrenal response to cytokines exerts an inhibitory feedback on the cell targets that mediate the behavioral effects of LPS and IL-1 beta.

scholarly journals Role of Interleukin-1.BETA. in Superovulation in Rats.

1997 ◽  
Vol 44 (6) ◽  
pp. 797-804 ◽  
Author(s):  
MIOKO ONO ◽  
YASUHIKO NAKAMURA ◽  
HIROSHI TAMURA ◽  
SHUJI TAKIGUCHI ◽  
NORIHIRO SUGINO ◽  
...  
Keyword(s):  
Interleukin 1 ◽  
Interleukin 1 Beta

Role of interleukin 1 beta in the regulation of rat intestinal multidrug resistance-associated protein 2 under conditions of experimental endotoxemia

Toxicology ◽  
2020 ◽  
Vol 441 ◽  
pp. 152527
Author(s):  
Maite Rocío Arana ◽  
Camila Juliana Dominguez ◽  
Felipe Zecchinati ◽  
Guillermo Nicolás Tocchetti ◽  
Aldo Domingo Mottino ◽  
...  
Keyword(s):  
Multidrug Resistance ◽  
Interleukin 1 ◽  
Interleukin 1 Beta ◽  
Experimental Endotoxemia

Differential effects of interleukin-1 alpha and interleukin-1 beta on human peripheral blood eosinophils

Blood ◽  
1989 ◽  
Vol 73 (7) ◽  
pp. 1904-1908 ◽  
Author(s):  
EA Whitcomb ◽  
CA Dinarello ◽  
SH Pincus
Keyword(s):  
Human Peripheral Blood ◽  
Interleukin 1 ◽  
Parasitic Infection ◽  
Human Monocyte ◽  
Enzyme Secretion ◽  
Interleukin 1 Beta ◽  
Disease States ◽  
Major Species ◽  
Blood Eosinophils

Abstract Interleukin-1 (IL-1) plays a major role in the response to infection, inflammation, and immunological challenge. Eosinophils participate in the host response to parasitic infection and allergic and hypersensitivity diseases. The role of IL-1 in these disease states has not been extensively explored. We have reported that purified human monocyte derived IL-1 (mIL-1), a mixture of the two IL-1 forms but predominantly consisting of IL-1 beta, modulates eosinophil oxidative metabolism and enzyme secretion. Although the two major species of IL-1 (IL-1 alpha and IL-1 beta) have identical specific activities on T cells, we now report the selective effects of human recombinant IL-1 (hrIL-1) alpha and hrIL-1 beta on eosinophil function. Whereas hrIL-1 beta caused a significant increase in arylsulfatase secretion (235.4 +/- 29% of resting secretion, P less than or equal to .01) and beta- glucuronidase secretion (135.8 +/- 9.6% of resting secretion, P less than or equal to .02) similar to our experience with mIL-1, hrIL-1 alpha had no effect on enzyme secretion. However, a mixture of hrIL-1 alpha and hrIL-1 beta reproduced the ability of mIL-1 to inhibit the oxidative response to suboptimal doses of phorbol myristate acetate (PMA). When eosinophils were separated into subpopulations by density gradients, we found that eosinophil responses to IL-1 differed among the populations. These results suggest that eosinophil subpopulations respond selectively to each form of IL-1.

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.

Effects of intracellular ions on interleukin-1 beta production by lipopolysaccharide-activated human monocytes

1992 ◽  
Vol 263 (5) ◽  
pp. C1073-C1080 ◽  
Author(s):  
U. Orlinska ◽  
R. C. Newton
Keyword(s):  
Culture Medium ◽  
Choline Chloride ◽  
Interleukin 1 ◽  
Disulfonic Acid ◽  
Interleukin 1 Beta ◽  
Activated Monocytes ◽  
Lps Activation ◽  
Intracellular Ions ◽  
Ionophore Monensin

Following the observation that interleukin 1 beta (IL-1 beta) production in lipopolysaccharide (LPS)activated monocytes increases in concert with a rise in intracellular pH (pHi), the role of ion transport in IL-1 beta production was investigated. The amiloride analogue 5-(N-ethyl-N-isopropyl)amiloride (EIPA), an inhibitor of the Na(+)-H+ antiporter, inhibited extracellular IL-1 beta. The replacement of Na+ in the culture medium with sucrose or choline chloride also prevented monocyte activation. The sodium ionophore monensin, in doses from 100 pM to 1 microM, potentiated LPS-stimulated extracellular IL-1 beta when compared with LPS alone. In the absence of LPS activation, monensin by itself at 10 nM stimulated IL-1 beta production to 63%. EIPA at 10 microM inhibited the Na+ influx, the rise in pHi, and intra- and extracellular IL-1 beta production in activated monocytes; this inhibition was reversed by 10 nM monensin. In the absence of bicarbonate, or in the presence of 10 microM 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid, the pHi of activated monocytes and the total protein synthesis did not change, but the production of IL-1 beta was inhibited. The data suggest that the stimulated influx of Na+ via the Na(+)-H+ antiporter regulates both pHi and IL-1 beta production in LPS-activated monocytes. The requirement for bicarbonate indicates an additional mechanism(s), separate from the modulation of pHi and intracellular Na+.

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