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At least 163 records · Page 9Linked to original sources
PubMed1984

Generation of an interleukin-I-like lymphocyte-stimulating factor at inflammatory sites: correlation with the infiltration of polymorphonuclear leucocytes.

Using a mouse thymocyte co-stimulation assay, we demonstrated thymocyte-stimulating activity in murine peritoneal fluid obtained from the early stage (3 to 9 h) of casein-induced inflammation. This early inflammatory stage coincided with the time at which an influx of polymorphonuclear leucocytes (PMN) into the inflamed site was observed. Similar thymocyte-stimulating activity was produced in vitro by PMN purified from 4-h peritoneal exudate but not by purified PMN obtained at a later stage (24 h) of the inflammation. The inflammatory factor was interleukin (IL)-I-like; it was devoid of IL-2 activity when tested with IL-2-dependent cells. It could stimulate murine thymocytes to produce IL-2. On a Sephadex G-75 column, the factor was eluted between the molecular sizes of 10 000 and 30 000; its peak activity was at 21 000. The factor mainly consisted of two (pI 6.5 and pI 5.0) iso-electrophoretically different factors.

Animals↗
PubMed1979

Inflammatory reactions and chemotactic factors.

Inflammatory reactions are mediated by a large number of chemical substances called chemical mediators, including chemotactic factors, which are released by immunologic as well as non-immunologic mechanisms. Chemotactic factors which act indirectly on target tissue can not only enhance inflammatory reactions (NCF-C) but may also eliminate the reactions (ECF-A).

Anaphylatoxins↗
PubMed2006

Inflammatory cytokine, growth factor and counterregulatory responses to exercise in children with type 1 diabetes and healthy controls.

In children with type 1 diabetes (T1DM), altered adaptive responses to exercise (secretion of growth factors, inflammatory cytokines, and glucoregulatory mediators) may have potential implications in growth and development, early onset of disease complications, and incidence of hypoglycemia. We therefore measured a broad spectrum of exercise responses in 12 children with T1DM (seven males and five females) and 12 controls (six males / six females) aged 11-15 yr, during a 30-min exercise challenge @ 80% VO(2)max. Euglycemia was strictly controlled during exercise, and in diabetic patients a basal rate of i.v. insulin was allowed to maintain baseline insulin concentrations. Throughout the experiment, interleukin-6 (IL-6) concentrations (pg/mL) were markedly higher in T1DM vs. controls (preexercise: 5.0+/-1.3 vs. 1.9+/-0.6, p<0.02; end-exercise 5.3+/-1.2 vs. 2.7+/-1.0, p<0.05; 30-min postexercise: 8.2+/-2.2 vs. 3.9+/-0.8, p<0.05). A similar pattern was also observed with norepinephrine. Growth hormone (GH) concentration was similar in both groups at baseline and end-exercise, but in T1DM the exercise-induced GH remained significantly elevated 30 min after exercise (9.2+/-2.2 vs. 3.1+/-0.9 ng/L, p<0.01). The exercise-induced increase in glucagon elicited by exercise in controls was similar to that previously observed in healthy adults (10+/-3 pg/mL); however, it was significantly blunted in T1DM children (2+/-2 pg/mL, p<0.05). In conclusion, T1DM children displayed significant alterations in multiple aspects of their adaptive response to intense exercise.

Adaptation, Physiological↗
PubMed1978

[Origin of a mitogrenic factor for cultivated macrophages (IMF: Inflammatory Mitogenic Factor) found in exudates of non-specific acute inflammation].

The mitogenic activity of inflammatory exudate obtained from irradiated Rats is reduced. After transfer of bone marrow syngeneic cells into irradiated Rats this mitogenic activity is further decreased, while after transfer of thymic cells it is increased. It is postulated that the mitogenic activity of inflammatory exudate could be related to thymic cells and that T lymphocytes may be involved in non specific-inflammatory reactions.

Acute Disease↗
PubMed2004

Thrombin peptide (TP508) promotes fracture repair by up-regulating inflammatory mediators, early growth factors, and increasing angiogenesis.

Previous studies have shown that a single injection of thrombin peptide (TP508) accelerates fracture repair in a closed rat femoral fracture model. The present study was conducted to elucidate the molecular mechanisms of TP508 action using Affymetrix genome-scale profiling and to link early gene expression changes to fracture histology and bone strength changes. Treatment of femoral fractures with TP508 accelerated fracture repair as determined by destructive torsion testing. Blinded histological analysis demonstrated that TP508-treated fracture callus had a significant increase in blood vessels relative to the controls. Gene array analysis showed that TP508 significantly induced expression of early growth factors, inflammatory response modifiers, and angiogenesis-related genes. This study therefore suggests that TP508 promotes fracture repair through a mechanism that involves an increased induction of a number of growth factors, enhanced expression of inflammatory mediators, and angiogenesis-related genes.

Animals↗
PubMed1997

Cytokines, nerve growth factor and inflammatory hyperalgesia: the contribution of tumour necrosis factor alpha.

1. Peripheral inflammation is characterized by heightened pain sensitivity. This hyperalgesia is the consequence of the release of inflammatory mediators, cytokines and growth factors. A key participant is the induction of the neurotrophin nerve growth factor (NGF) by interleukin-1 beta (IL-1 beta). 2. Tumour necrosis factor alpha (TNF alpha) has been shown both to produce hyperalgesia and to upregulate IL-1 beta. We have now examined whether the induction of TNF alpha in inflammatory lesions contributes to inflammatory sensory hypersensitivity by inducing IL-1 beta and NGF. 3. The intraplantar injection of complete Freund's adjuvant (CFA) in adult rats produced a localized inflammation of the hindpaw with a rapid (3 h) reduction in withdrawal time in the hot plate test and in the mechanical threshold for eliciting the flexion withdrawal reflex. 4. The CFA-induced inflammation resulted in significant elevation in the levels of TNF alpha, IL-1 beta and NGF in the inflamed paw. In the case of TNF alpha, an elevation was detected at 3 h, rose substantially at 6 h, peaked at 24 h and remained elevated at 5 days, with similar but smaller changes in the contralateral non-inflamed hindpaw. No increase in serum TNF alpha was detected at 24 h post CFA injection. 5. Intraplantar recombinant murine TNF alpha injections produce a short-lived (3-6 h) dose-dependent (50-500 ng) increase in thermal and mechanical sensitivity which was significantly attenuated by prior administration of anti-NGF antiserum. 6. Intraplantar TNF alpha (100-500 ng) also elevated at 6 but not 48 h the levels of IL-1 beta and NGF in the hindpaw. 7. A single injection of anti-TNF alpha antiserum, 1 h before the CFA, at a dose sufficient to reduce the effects of a 100 ng intraplantar injection of TNF alpha, significantly delayed the onset of the resultant inflammatory hyperalgesia and reduced IL-1 beta but not NGF levels measured at 24 h. 8. The elevation of TNF alpha in inflammation, by virtue of its capacity to induce IL-1 beta and NGF, may contribute to the initiation of inflammatory hyperalgesia.

Animals↗
PubMed1998

Synergistic upregulation of metalloproteinase-9 by growth factors and inflammatory cytokines: an absolute requirement for transcription factor NF-kappa B.

Matrix metalloproteinase (MMPs) enzymes are implicated in matrix remodelling during proliferative inflammatory processes including wound healing. We report here synergistic upregulation of MMP-9 protein and mRNA by platelet-derived growth factor (PDGF) or basic fibroblast growth factor (bFGF) in combination with interleukin-1alpha (IL-1alpha) or tumour necrosis factor-alpha (TNF-alpha) in primary rabbit and human dermal fibroblasts. The synergistic interaction between growth factors and cytokines implies that basement membrane remodelling is maximal physiologically when both are present together. The signalling pathways mediating this synergistic regulation are not understood, although analysis of the MMP-9 promoter has identified an essential proximal AP-1 element and an upstream nuclear factor kappa-B (NF-kappaB) site. Using electromobility shift assays, binding to the AP-1 site was only slightly increased by growth factors and cytokines. NF-kappaB binding was rapidly induced by IL-1alpha or TNF-alpha but was neither induced nor potentiated by bFGF or PDGF. Neither AP-1 nor NF-kappaB was therefore sufficient on its own for synergistic regulation. Using a recently developed adenovirus that overexpresses the inhibitory subunit, IkappaB alpha, we demonstrated an absolute requirement for NF-kappaB in upregulation of MMP-9. Activation of NF-kappaB binding by inflammatory cytokines was therefore necessary but not sufficient for synergistic upregulation of MMP-9.

Animals↗
PubMed1992

Circulating von Willebrand factor in inflammatory bowel disease.

Raised circulating von Willebrand factor is a recognised marker of vascular injury. To evaluate the role of vascular injury in the pathogenesis of inflammatory bowel disease, serum von Willebrand factor in Crohn's disease, ulcerative colitis, confirmed bacterial diarrhoea, and healthy subjects was measured. von Willebrand factor values were raised in 9/14 patients (p = 0.007) with active Crohn's disease, 15/28 (p = 0.0004) with inactive Crohn's disease, 16/23 (p = 0.0003) with active ulcerative colitis, 9/27 (p = 0.04) with inactive ulcerative colitis, and 15/17 (p = 0.0001) patients with bacterial diarrhoea. Serum von Willebrand factor was unrelated to disease activity in Crohn's disease but was significantly raised in active (p = 0.02) compared with inactive ulcerative colitis. In contrast to controls, the detection of von Willebrand factor from inflammatory bowel disease sera and that from fractured endothelial cells was significantly inhibited by the reducing agent, dithiothreitol, suggesting the presence of an additional dithiothreitol sensitive form of the molecule derived from injured endothelial cells in inflammatory bowel disease. That serum von Willebrand factor is raised in quiescent as well as active Crohn's disease is compatible with the proposal that vascular injury is a fundamental abnormality in this disorder. The raised von Willebrand factor values in active inflammatory bowel disease and bacterial diarrhoea could be caused by either vascular injury, occurring secondary to bowel inflammation, or to an acute phase response resulting from endothelial cell stimulation by mediators released during the inflammatory process. Raised circulating von Willebrand factor could contribute to the increased risk of thrombosis associated with active inflammatory bowel disease.

Bacterial Infections↗
PubMed1999

Vegetarians and cardiovascular risk factors: hemostasis, inflammatory markers and plasma homocysteine.

We studied hemostatic and inflammatory cardiovascular risk factors (CVRF), and total plasma homocysteine (tHcy) in 26 vegetarians (23 lacto- or ovolactovegetarians and 3 vegans), matched by age, sex and socioeconomic status with omnivorous controls. Vegetarians had significantly lower proportion of eicosapentaenoic (EPA) and docosahexaenoic (DHA) acids in plasma lipids, significantly shortened bleeding time, and increased blood platelet count and in vitro platelet function (aggregation and secretion). Plasma levels of all coagulation or fibrinolytic factors and natural inhibitors synthesized in the liver were lower in vegetarians than in controls. Whereas for some factors this decrease was statistically significant (fibrinogen, factor VIIc, antithrombin III, protein S, plasminogen) for the remaining (factors VIIIc, Vc, prothrombin, protein C) a trend in the same direction was found. For hemostatic proteins of predominantly extrahepatic origin (von Willebrand factor. tPA, PAI-1) this tendency was not present. No significant differences in inflammatory proteins (C-reactive protein and alpha1-protease inhibitor) were detected in both groups. tHcy was significantly increased in vegetarians, and correlated only with cobalamin levels. The increased platelet function and tHcy found in vegetarians may counteract the known cardiovascular health benefits of vegetarian diet (VD).

Adult↗
PubMed1998

Increased levels of soluble tumor necrosis factor receptors in atherosclerosis: no clear relationship with levels of tumor necrosis factor.

Inflammatory mediators, such as tumor necrosis factor alpha (TNF), may be important in the pathogenesis of atherosclerosis. Interactions between TNF and its target cell(s) requires the presence of specific receptors on the latter. Plasma levels of the two soluble forms of these receptors (tumor necrosis factor receptors, (sTNFr)) and TNF itself were measured by ELISA in 20 patients with peripheral vascular disease (PVD), 20 survivors of a myocardial infarction, and 20 age and sex matched controls. Levels of the p55 variant of the sTNFr were unchanged but levels of the p75 variant were increased in both groups of patients (ANOVA both P < 0.01). TNF was also raised in both groups of patients (both P < 0.05) but levels did not correlate with either sTNFr. In atherosclerosis, increased levels of p75 sTNFr may be further evidence of inappropriate leukocyte activation but unlikely to modulate the effect of free plasma TNF.

Aged↗