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At least 325 records · Page 18Linked to original sources
PubMed1990

Effect of tenoxicam on inflammation and immune cellular function.

1. We have shown that nonsteroidal anti-inflammatory drugs are potent inhibitors of neutrophil activation. Tenoxicam is a new compound of the oxicam family which has been shown to be effective for routine clinical use. 2. In the present study we examined the immune pharmacological effects of this compound on lymphocyte function by determining its effect on the expression of IL-2 receptors, on monocyte function by looking at chemotaxis and IL-1 release and on neutrophil function by evaluating the chemotactic response to a standard stimulus. 3. The data show that Tenoxicam inhibits the neutrophil and monocyte functional chemotactic response in vitro, and to some extent in vivo for monocytes, but has no effect on the expression of IL-2 receptors or IL-1 release. Tenoxicam inhibits the mobilization of neutrophils and monocytes to inflammatory sites, even though this effect was not clearly demonstrable when cells were tested after oral use.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed2004

Evidence for a role of macrophage migration inhibitory factor in vascular disease.

OBJECTIVE: Inflammation plays an essential role in atherosclerosis and restenosis. Macrophage migration inhibitory factor (MIF) is a proinflammatory cytokine that is widely expressed in vascular cells. However, there is no in vivo evidence that MIF participates directly in vascular injury and repair. Therefore, we investigated the effect of MIF blockade on the response to experimental angioplasty in atherosclerosis-susceptible mice. METHODS AND RESULTS: Carotid artery dilation (2.5 atm) and complete endothelial denudation were performed in male C57BL/6J LDL receptor-deficient mice treated with a neutralizing anti-MIF or isotype control monoclonal antibody. After 7 days and 28 days, intimal and medial sizes were measured and intima/media area ratio (I/M) was calculated. Intimal thickening and I/M were reduced significantly by anti-MIF compared with control antibody. Vascular injury was accompanied by progressive vessel enlargement or "positive remodeling" that was comparable in both treatment groups. MIF blockade was associated with reduced inflammation and cellular proliferation and increased apoptosis after injury. CONCLUSIONS: Neutralizing MIF bioactivity after experimental angioplasty in atherosclerosis-susceptible mice reduces vascular inflammation, cellular proliferation, and neointimal thickening. Although the molecular mechanisms responsible for these effects are not yet established, these data prompt further research directed at understanding the role of MIF in vascular disease and suggest novel therapeutic interventions for preventing atherosclerosis and restenosis.

Angioplasty, Balloon↗
PubMed2004

Cellular proteolysis and systemic inflammation during exacerbation in cystic fibrosis.

BACKGROUND: Weight loss indicates a poor prognosis in cystic fibrosis (CF). We hypothesised that fat-free mass (FFM) depletion and increased systemic inflammation would be associated with increased cellular proteolysis during an exacerbation of the respiratory symptoms. Patients were studied prospectively from the beginning of treatment with antibiotics when admitted to the Adults CF Centre. METHODS: Twenty six patients with CF were studied at the start and end of antibiotic treatment and 2 weeks later. Mean (95% CI) FEV1 when clinically stable was 54.1 (44.5, 62.6)% predicted. Urinary excretion of Pseudouridine (5-ribosyluracil, PSU) was determined as an indicator of cellular protein breakdown. Body composition was assessed by dual energy X-ray absorptiometry (DXA). RESULTS: Patients had increased concentrations of PSU at all assessments (p<0.01). Those with a low FFM had greater PSU (ratio to FFMI) than those with a normal FFM at all assessments. At the start of treatment, PSU was related to FFM, C-reactive protein (CRP) (p<0.05) and tumour necrosis factor (TNF)alpha soluble receptors (sr) I and II (p<0.01). Circulating inflammatory mediators were greater in patients than in healthy subjects at all assessments. CONCLUSION: Increased protein breakdown is associated with a low FFM and increased systemic inflammation and it may be a contributory mechanism of poor weight preservation in CF.

Absorptiometry, Photon↗
PubMed1989

Cellular and molecular aspects of granulomatous inflammation.

Recent advances in cellular and molecular biology have provided important new avenues to assess mechanisms of granuloma formation/regulation. For example, current studies have identified various cytokines that can exert a powerful influence on both immune and non-immune cells and dictate inflammatory processes. Some of these cytokines are potentially active during the initiation and maintenance of chronic inflammation, including tumor necrosis factor, interleukin 1, and a novel class of chemotactic cytokines. This latter group of mediators belongs to a super-gene family of immune signals that play a key role in the selective recruitment of inflammatory cells to an area of inflammation. The coordinated synthesis of these cytokines is likely important to the development of the granulomatous response. The participation of molecular signals produced by non-inflammatory cells, fibroblasts, and epithelial cells, also warrants special consideration. These "bystander" cells appear to possess effector cell functions and likely serve an important role in inducing pulmonary granulomatous inflammation. Thus, a clear understanding of the cells and molecular signals involved in the initiation and maintenance of chronic pulmonary inflammation will be necessary to assess lesion development and design more selective/effective therapies.

Animals↗
PubMed1989

Pharmacological investigation of acute cellular accumulation in immunological air pouch inflammation.

Immunologically-mediated cellular accumulation was measured 24 hours after antigenic challenge using a rat subcutaneous air pouch model. This response was inhibited by treatment with prednisolone, colchicine, anti-thymocyte serum and systemic antigen. In contrast, administration of a range of other pharmacological and clinically active agents had little effect. The profile of inhibitory activity suggested that this response was mainly due to delayed type hypersensitivity with little anaphylactic or Arthus-type component.

4,5-Dihydro-1-(3-(trifluoromethyl)phenyl)-1H-pyraz↗
PubMed2001

Cellular markers of systemic inflammation and immune suppression in patients with organ failure due to severe acute pancreatitis.

BACKGROUND: Few data are available on cellular markers of systemic inflammation and immune suppression in early acute pancreatitis. The aim of this study was to describe the cellular immune inflammatory status of patients with acute pancreatitis in relation to development of organ failure. METHODS: Prospective study including 89 patients who presented within 72 h of onset of pain. Fifty-eight of them had mild disease (Grade I group), 19 had severe disease with no organ dysfunction (Grade II group) and 12 had severe disease with organ dysfunction (Grade III group). Serial blood samples were collected on admission and following 2 days. Phagocyte surface markers were analysed using flow cytometry. RESULTS: The proportion of HLA-DR-positive monocytes, a marker of immune suppression, and CD11b expression level on neutrophils and monocytes, a marker of systemic inflammation, were related to Grades I-III (P for trend <0.001). In Grade III patients, the proportion of HLA-DR-positive monocytes was low on presentation, or decreased rapidly during follow-up, whereas CD11b expression levels were persistently high. L-selectin and monocyte CD14 expression levels were not related to disease severity. CONCLUSIONS: Immune suppression develops early, rapidly and unexpectedly in patients with acute pancreatitis. Monitoring immune inflammatory status may provide the means by which to identify patients who benefit from biological response modifier therapy.

Acute Disease↗
PubMed2005

Role of cytokines in cardiovascular diseases: a focus on endothelial responses to inflammation.

Complex cellular and inflammatory interactions are involved in the progress of vascular diseases. Endothelial cells, upon exposure to cytokines, undergo profound alterations of function that involve gene expression and de novo protein synthesis. The functional reprogramming of endothelial cells by cytokines is of importance especially in patients with chronic vascular inflammation. The intercellular network of dendritic cells, T-lymphocytes, macrophages and smooth muscle cells generates a variety of stimulatory cytokines [e.g. TNF-alpha (tumour necrosis factor-alpha), IL (interleukin)-1, IL-6 and IFN-gamma (interferon-gamma)] and growth factors that promote the development of functional and structural vascular changes. High concentrations of proinflammatory cytokines increase oxidative stress, down-regulate eNOS (endothelial nitric oxide synthase) bioactivity and induce endothelial cell apoptosis. Chemoattractant cytokines [e.g. VEGF (vascular endothelial growth factor), TGF-beta1 (transforming growth factor-beta1) and IL-8] are important regulators of inflammation-induced angiogenesis and are directly modulated by nitric oxide. This review will focus on the vascular mechanisms orchestrated by cytokines and summarizes the current knowledge concerning the contribution of cytokines to cardiovascular diseases.

Cardiovascular Diseases↗
PubMed2001

Relationship between airway inflammation, hyperresponsiveness, and obstruction in asthma.

BACKGROUND: Although the role of eosinophils in airway inflammation in chronic asthma has been extensively studied, a role for neutrophils has not been well characterized. Furthermore, prior studies have not systematically sought or controlled for factors that might confound the relationship between cellular markers of inflammation and physiologic measures of airway function. OBJECTIVE: The purpose of this study was to determine whether eosinophilic and neutrophilic inflammation independently contribute to abnormalities of airway function in asthma. METHODS: Multivariate analysis of data collected during screening and enrollment of 205 asthmatic adults for clinical trials was conducted to examine the relationships between cellular inflammation in induced sputum and FEV(1) and methacholine responsiveness (PC(20)) while confounding factors were controlled for. RESULTS: We found that age, sex, ethnicity, and use of inhaled corticosteroids were important confounding factors of the relationship between cellular inflammation and airway function. When these factors were controlled for, multivariate analysis showed that eosinophil percentage in induced sputum is independently associated with lower FEV(1) and lower PC(20) (P = .005 and P = .005, respectively). In the same models, increased sputum neutrophil percentage is independently associated with lower FEV(1) (P = .038) but not with PC(20) (P = .49). CONCLUSIONS: These results suggest that both eosinophilic inflammation and neutrophilic inflammation independently contribute to abnormalities of FEV(1) in asthma. Therapies directed specifically at control of neutrophilic inflammation might be useful in improving airway caliber in patients with chronic asthma.

Adult↗
PubMed1994

[How do we define inflammation?].

Nowadays inflammation is commonly defined as a defensive reaction involving the immune system. This paper clarifies the historical roots of this definition. The Russian embryologist Metchnikoff made--100 years ago--the initial observations on phagocytosis that provided a definition of inflammation based on a cellular theory of immunity. Following the many attacks by those who favored the view that immunity was based upon humoral mechanisms, Bordet argued that Metchnikoff's cellular theory of inflammation could be reconciled with the theory of humoral immunity. This study helps the modern reader to grasp the theoretical assumptions supporting our concept of inflammation.

Europe↗