scholarly journals Recombinant interleukin-1  dilates steelhead trout coronary microvessels: effect of temperature and role of the endothelium, nitric oxide and prostaglandins

2015 ◽  
Vol 218 (14) ◽  
pp. 2269-2278 ◽  
Author(s):  
I. A. S. F. Costa ◽  
T. W. Hein ◽  
C. J. Secombes ◽  
A. K. Gamperl
Keyword(s):  
Nitric Oxide ◽  
Interleukin 1 ◽  
Effect Of Temperature ◽  
Steelhead Trout

scholarly journals Regulation of matrix turnover in meniscal explants: role of mechanical stress, interleukin-1, and nitric oxide

2003 ◽  
Vol 95 (1) ◽  
pp. 308-313 ◽  
Author(s):  
Sang-jin Shin ◽  
Beverley Fermor ◽  
J. Brice Weinberg ◽  
David S. Pisetsky ◽  
Farshid Guilak
Keyword(s):  
Nitric Oxide ◽  
Mechanical Stress ◽  
Dynamic Compression ◽  
Interleukin 1 ◽  
Joint Disease ◽  
Proteoglycan Synthesis ◽  
Compressive Stresses ◽  
Nitric Oxide Synthase 2 ◽  
Oxide Synthase

The meniscus is an intra-articular fibrocartilaginous structure that serves essential biomechanical roles in the knee. With injury or arthritis, the meniscus may be exposed to significant changes in its biochemical and biomechanical environments that likely contribute to the progression of joint disease. The goal of this study was to examine the influence of mechanical stress on matrix turnover in the meniscus in the presence of interleukin-1 (IL-1) and to determine the role of nitric oxide (NO) in these processes. Explants of porcine menisci were subjected to dynamic compressive stresses at 0.1 MPa for 24 h at 0.5 Hz with 1 ng/ml IL-1, and the synthesis of total protein, proteoglycan, and NO was measured. The effects of a nitric oxide synthase 2 (NOS2) inhibitor were determined. Dynamic compression significantly increased protein and proteoglycan synthesis by 68 and 58%, respectively, compared with uncompressed explants. This stimulatory effect of mechanical stress was prevented by the presence of IL-1 but was restored by specifically inhibiting NOS2. Release of proteoglycans into the medium was increased by IL-1 or mechanical compression and further enhanced by IL-1 and compression together. Stimulation of proteoglycan release in response to compression was dependent on NOS2 regardless of the presence of IL-1. These finding suggest that IL-1 may modulate the effects of mechanical stress on extracellular matrix turnover through a pathway that is dependent on NO.

scholarly journals Human astrocytes inhibit Cryptococcus neoformans growth by a nitric oxide-mediated mechanism.

1994 ◽  
Vol 180 (1) ◽  
pp. 365-369 ◽  
Author(s):  
S C Lee ◽  
D W Dickson ◽  
C F Brosnan ◽  
A Casadevall
Keyword(s):  
Nitric Oxide ◽  
Cryptococcus Neoformans ◽  
Interleukin 1 ◽  
Primary Cultures ◽  
Immune Deficiency Syndrome ◽  
Deficiency Syndrome ◽  
Effector Cells ◽  
Human Astrocytes ◽  
Life Threatening

Cryptococcus neoformans is an opportunistic fungus that causes life-threatening meningoencephalitis in 5-10% of patients with acquired immune deficiency syndrome. Cryptococcal meningoencephalitis is characterized by a lymphohistiocytic infiltrate, accumulation of encapsulated forms of C. neoformans, and varying degrees of glial reaction. Little is known about the contribution of endogenous central nervous system cells to the pathogenesis of cryptococcal infections. In this study, we investigated the role of astrocytes as potential effector cells against C. neoformans. Primary cultures of human fetal astrocytes, activated with interleukin 1 beta plus interferon gamma inhibited the growth of C. neoformans. The inhibition of C. neoformans growth was paralleled by production of nitrite, and reversed by the inhibitors of nitric oxide (NO.) synthase, NG-methyl-mono-arginine and NG-nitro-arginine methyl ester. The results suggest a novel function for human astrocytes in host defence and provide a precedent for the use of NO. as an antimicrobial effector molecule by human cells.

Interleukin 1 and endotoxin activate soluble guanylate cyclase in vascular smooth muscle

1990 ◽  
Vol 259 (1) ◽  
pp. R38-R44 ◽  
Author(s):  
D. Beasley
Keyword(s):  
Nitric Oxide ◽  
Guanylate Cyclase ◽  
Soluble Guanylate Cyclase ◽  
Interleukin 1 ◽  
Physiological Salt Solution ◽  
Initial Exposure ◽  
Vasodilatory Action ◽  
Ly 83583

Our recent studies indicate that interleukin 1 (IL-1) and bacterial lipopolysaccharide inhibit agonist-induced contractions in rat aortic rings by an endothelium-independent mechanism. The present study investigated the role of guanosine 3',5'-cyclic monophosphate (cGMP) in the vasodilatory action of IL-1 and endotoxin. Rat aortic rings were denuded of endothelium and incubated for 3 h in physiological salt solution containing no additions, IL-1 (20 ng/ml), or endotoxin (10 micrograms/ml). Contractions induced by phenylephrine (3 x 10(-7) M) were decreased by 40 and 85% in endotoxin- and IL-1-treated rings, respectively. IL-1 increased cGMP content 2.5-fold in the absence of and 5.5-fold in the presence of 3-isobutyl-1-methylxanthine (IBMX). Endotoxin also increased cGMP content in the absence and presence of IBMX (5.5- and 25-fold, respectively). Both IL-1- and endotoxin-induced increases in cGMP occurred 3-4 h after initial exposure. The guanylate cyclase inhibitors, LY 83583 and methylene blue, each abolished IL-1- and endotoxin-induced inhibition of contraction and IL-1-induced production of cGMP. Furthermore, hemoglobin, which binds nitric oxide, completely blocked IL-1-induced increases in cGMP. We conclude that IL-1 and endotoxin inhibit vascular contraction in vitro by increasing aortic cGMP content. Studies with inhibitors suggest IL-1 and endotoxin may induce endothelium-independent production of nitric oxide or another free radical that activates soluble guanylate cyclase.

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