In vivo changes in plasma acute phase protein levels in the rat induced by slow release of IL‐1, IL‐6 and TNF

Lewis, E. J.; Sedgwick, A. D.; Hanahoe, T.H.P.

doi:10.1155/s0962935192000085

Cited by 12 publications

(5 citation statements)

References 1 publication

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The liver is the major source of serum CP in adults [13]. The synthesis of serum CP in hepatic cells is increased by proinflammatory agonists [14–16]. The recent research has indicated that increased ceruloplasmin concentrations were associated with an increased risk of myocardial infarction and stroke [17, 18].…”

Section: Discussionmentioning

confidence: 99%

Ceruloplasmin and the Extent of Heart Failure in Ischemic and Nonischemic Cardiomyopathy Patients

Zhou

et al. 2013

Mediators of Inflammation

View full text Add to dashboard Cite

Objective. Ceruloplasmin was elevated in patients with coronary heart disease, but the relationship between ceruloplasmin and heart failure was still unknown. We aimed to evaluate ceruloplasmin in heart failure patients and assess association between ceruloplasmin and the extent of heart failure. Methods and Results. 202 heart failure patients were divided into ischemic (78 with coronary stenosis) and nonischemic groups (124 without coronary stenosis). 94 subjects without heart failure were included as controls. The extent of heart failure was defined according to NYHA classification. Ceruloplasmin levels in ischemic (P < 0.001) and nonischemic groups (P < 0.001) were higher than those in control group. Ceruloplasmin had a positive linear correlation with C-reactive protein (P < 0.01) and a negative linear correlation with LVEF (P < 0.05). In nonischemic group, CP levels were significantly different among different NYHA subgroups (P < 0.05). The correlation between ceruloplasmin and extent of heart failure was calculated by binary logistic regression. Ceruloplasmin showed an independent association with the extent of heart failure in nonischemic cardiomyopathy patients (P < 0.05). Conclusions. Ceruloplasmin was significantly elevated in patients with ischemic or nonischemic cardiomyopathy and had linear correlation with C-reactive protein and LVEF. In nonischemic cardiomyopathy patients, the ceruloplasmin value was an independent biomarker associated with the extent of heart failure.

show abstract

Section: Discussionmentioning

confidence: 99%

Ceruloplasmin and the Extent of Heart Failure in Ischemic and Nonischemic Cardiomyopathy Patients

Zhou

et al. 2013

Mediators of Inflammation

View full text Add to dashboard Cite

show abstract

“…15-17 IL-6 is a major mediator of inflammation, 39 inducing the synthesis of acute-phase proteins in the liver. 40 In addition, IL-6 induces myoblast proliferation in culture, 41 suggesting that the observed increments in this cytokine may influence skeletal muscle regeneration after snake venominduced myonecrosis. IL-1b plays a number of roles in inflammation, inducing the expression of adhesion molecules, 42 and the release of leukocyte chemotactic factors, 43 besides altering the functional properties of endothelial cells.…”

Section: Discussionmentioning

confidence: 99%

Increments in cytokines and matrix metalloproteinases in skeletal muscle after injection of tissue‐damaging toxins from the venom of the snake Bothrops asper

Rucavado

Escalante

Teixeira

et al. 2002

Mediators of Inflammation

130

View full text Add to dashboard Cite

Envenomations by the snake Bothrops asper are characterized by prominent local tissue damage (i.e. myonecrosis), blistering, hemorrhage and edema. Various phospholipases A2 and metalloproteinases that induce local pathological alterations have been purified from this venom. Since these toxins induce a conspicuous inflammatory response, it has been hypothesized that inflammatory mediators may contribute to the local pathological alterations described. This study evaluated the local production of cytokines and matrix metalloproteinases (MMPs) as a consequence of intramuscular injections of an Asp-49 myotoxic phospholipase A2 (myotoxin III (MT-III)) and a P-I type hemorrhagic metalloproteinase (BaP1) isolated from B. asper venom. Both enzymes induced prominent tissue alterations and conspicuous increments in interleukin (IL)-1beta, IL-6 and a number of MMPs, especially gelatinase MMP-9, rapidly after injection. In contrast, no increments in tumor necrosis factor-alpha (TNF-alpha) and interferon-gamma were detected. In agreement, MT-III and BaP1 did not induce the synthesis of TNF-alpha by resident peritoneal macrophages in vitro. Despite the conspicuous expression of latent forms of MMPs in muscle, evidenced by zymography, there were no increments in activated MMP-2 and only a small increase in activated MMP-9, as detected by a functional enzymatic assay. This suggests that MMP activity was regulated by a highly controlled activation of latent forms and, probably, by a concomitant synthesis of MMP inhibitors. Since no hemorrhage nor dermonecrosis were observed after injection of MT-III, despite a prominent increase in MMP expression, and since inflammatory exudate did not enhance hemorrhage induced by BaP1, it is suggested that endogenous MMPs released in the tissue are not responsible for the dermonecrosis and hemorrhage characteristic of B. asper envenomation. Moreover, pretreatment of mice with the peptidomimetic MMP inhibitor batimastat did not reduce myotoxic nor edema-forming activities of MT-III, suggesting that MMPs do not play a prominent role in the pathogenesis of these effects in this experimental model. It is concluded that MT-III and BaP1 induce a local inflammatory response associated with the synthesis of IL-1beta, IL-6 and MMPs. MMPs do not seem to play a prominent role in the acute local pathological alterations induced by these toxins in this experimental model.

show abstract

“…In vitro data have suggested that there are two types of APPs, type 1 are stimulated by IL-1 (a or b, TNFa) and enhanced by IL-6, whilst type 2 are induced by interleukin-6 (or IL-11, leukaemia inhibitory factor, oncostatin M, ciliary neutrophilic factor) [31]. Analysis of isolated or cultured hepatocytes stimulated by the different cytokines/steroids has demonstrated that caeruloplasmin synthesis is induced by IL-6, rat haptoglobin by IL-1 and enhanced by IL-6, albumin synthesis is reduced by IL-1 and stimulated by glucocorticoids [15,32,33]. Seromucoid is a mixture of a 1 acid glycoprotein, a 1 cysteine protease inhibitor and hemopexin and from in vivo experiments would appear to be mainly dependent on the IL-1 type cytokines.…”

Section: Discussionmentioning

confidence: 99%

“…Therefore assays for a variety of rat APPs were developed/modified to monitor plasma protein changes in inflammation induced models [14]. These assays have been used previously to study APP induction by interleukin-1, interleukin-6 and tumour necrosis factor [15].…”

Section: Introductionmentioning

confidence: 99%

A simple inflammation model that distinguishes between the actions of anti-inflammatory and anti-rheumatic drugs

Lewis

Bishop

Aspinall

1998

Inflammation Research

Self Cite

View full text Add to dashboard Cite

show abstract

In vivo changes in plasma acute phase protein levels in the rat induced by slow release of IL‐1, IL‐6 and TNF

Cited by 12 publications

References 1 publication

Ceruloplasmin and the Extent of Heart Failure in Ischemic and Nonischemic Cardiomyopathy Patients

Ceruloplasmin and the Extent of Heart Failure in Ischemic and Nonischemic Cardiomyopathy Patients

Increments in cytokines and matrix metalloproteinases in skeletal muscle after injection of tissue‐damaging toxins from the venom of the snake Bothrops asper

A simple inflammation model that distinguishes between the actions of anti-inflammatory and anti-rheumatic drugs

Contact Info

Product

Resources

About