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Search Results: 1 - 10 of 297666 matches for " Evangelos J Giamarellos-Bourboulis "
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Obesity as a Consequence of Gut Bacteria and Diet Interactions
Katerina Kotzampassi,Evangelos J. Giamarellos-Bourboulis,George Stavrou
ISRN Obesity , 2014, DOI: 10.1155/2014/651895
Abstract: Obesity is a major public health concern, caused by a combination of increased consumption of energy-dense foods and reduced physical activity, with contributions from host genetics, environment, and adipose tissue inflammation. In recent years, the gut microbiome has also been found to be implicated and augmented research in mice and humans have attributed to it both the manifestation and/or exacerbation of this major epidemic and vice versa. At the experimental level, analysis of fecal samples revealed a potential link between obesity and alterations in the gut flora (drop in Bacteroidetes and increase in Firmicutes), the specific gut microbiome being associated with the obese phenotype. Conventionally raised mice were found to have over 40% more total body fat compared with those raised under germ-free conditions, while conventionalization of germ-free mice resulted in a significant increase in total body fat. Similarly, the sparse data in humans supports the fact that fat storage is favoured by the presence of the gut microbiota, through a multifaceted mechanism. Efforts to identify new therapeutic strategies to modulate gut microbiota would be of high priority for public health, and to date, probiotics and/or prebiotics seem to be the most effective tools. 1. Introduction Obesity is a major public health concern, threatening both the industrialized and the developing countries, largely in parallel to the adoption of a “modern”/Western-type lifestyle. It results from a long-term disbalance between energy intake and expenditure, that is, increased consumption of more energy-dense, nutrient-poor foods containing high levels of sugar and saturated fats in combination with reduced physical activity [1]. However, the mechanisms underlying obesity seem to be far from the long-held belief in caloric intake and lifestyle factors. It is becoming evident that obesity and its causes are significantly more complex than previously thought, with contributions from host genetics, environment, diet and lifestyle, and systemic and adipose tissue inflammation [2]. Obesity is now characterized by a cluster of important chronic metabolic disorders, including insulin resistance, type 2 diabetes, fatty liver disease, atherosclerosis, hypertension, and hypercholesterolemia, and by a low grade of systemic inflammation [3], being the cause of exacerbation of all the above and leading to increased morbidity and mortality. Moreover, obesity is detrimental to the quality of life as a whole and implies high health costs as a consequence of its associated morbidities. In recent
Dexamethasone Down-Regulates Expression of Triggering Receptor Expressed on Myeloid Cells-1: Evidence for a TNFα-Related Effect
Ira Mihailidou,Aimilia Pelekanou,Aikaterini Pistiki,Aikaterini Spyridaki,Georgia Damoraki,Evangelos J. Giamarellos-Bourboulis
Frontiers in Public Health , 2013, DOI: 10.3389/fpubh.2013.00050
Abstract: Objectives: To investigate the effect of dexamethasone on triggering receptor expressed on myeloid cells-1 (TREM-1).
The Importance of Fever as a Predictive Symptom for the Potency of Host's Monocytes to Release Pro- and Anti-Inflammatory Mediators
Magdalini Kyriakopoulou,Anastasia Antonopoulou,Maria Raftogiannis,Fotini Baziaka,Thomas Tsaganos,Kyriaki Kanellakopoulou,Evangelos J. Giamarellos-Bourboulis
Mediators of Inflammation , 2008, DOI: 10.1155/2008/450196
Abstract: Objective. To clarify whether time lapsing from advent of fever as a first sign of sepsis may be indicative of the potency of monocytes for the release of pro- and anti-inflammatory mediators. Methods. Monocytes were isolated from blood of 51 septic patients and 9 healthy donors. Monocytes were incubated in the absence and presence of patients' serum and concentrations of tumour necrosis factor-alpha (TNF), interleukin (IL)-6, IL-10, and malondialdehyde (MDA) were estimated in supernatants. Patients were divided into three groups: group A: <12 hours; group B: 12–24 hours, and group C: >24 hours between initiation of fever and blood sampling. Results. TNF of supernatants of groups B and C was higher than controls, as also were IL-6 of A and C, IL-10 of A and B, and MDA of A. IL-6 of group A was increased after addition of patients serum. A negative correlation was found between time from initiation of symptoms and IL-6 of monocyte supernatants incubated in the presence of patients serum. Median IL-6 of survivors was higher than nonsurvivors. Conclusion. Monocytes are potent for the release of pro- and anti-inflammatory mediators within the first 24 hours upon advent of fever related to sepsis; serum stimulates further release of IL-6 within the first 12 hours.
The level of hypotension during hemorrhagic shock is a major determinant of the post-resuscitation systemic inflammatory response: an experimental study
Emmanuel E Douzinas, Ilias Andrianakis, Olga Livaditi, Pantelis Paneris, Marios Tasoulis, Aimilia Pelekanou, Alex Betrosian, Evangelos J Giamarellos-Bourboulis
BMC Physiology , 2008, DOI: 10.1186/1472-6793-8-15
Abstract: Fifteen rabbits were equally allocated into three groups: sham-operated (group sham); bled within 30 minutes to mean arterial pressure (MAP) of 40 mmHg (group shock-40); bled within 30 minutes to MAP of 30 mmHg (group shock-30). Shock was maintained for 60 min. Resuscitation was performed by reinfusing shed blood with two volumes of Ringer's lactate and blood was sampled for estimation of serum levels aminotransferases, creatinine, TNF-α, IL-1β, IL-6, malondialdehyde (MDA) and total antioxidant status (TAS) and for the determination of oxidative burst of polymorhonuclears (PMNs) and mononuclear cells (MCs).Serum AST of group shock-30 was higher than that of group shock-40 at 60 and 120 minutes after start of resuscitation; serum creatinine of group shock-30 was higher than group shock-40 at 120 minutes. Measured cytokines, MDA and cellular oxidative burst of groups, shock-40 and shock-30 were higher than group sham within the first 60 minutes after start of resuscitation. Serum concentrations of IL-1β, IL-6 and TNF-α of group shock-30 were higher than group shock-40 at 120 minutes (p < 0.05). No differences were found between two groups regarding serum MDA and TAS and oxidative burst on PMNs and MCs but both groups were different to group sham.The level of hypotension is a major determinant of the severity of hepatic and renal dysfunction and of the inflammatory response arising during post-ischemic hemorrhagic shock resuscitation. These findings deserve further evaluation in the clinical setting.Hemorrhagic shock is conceived as an insult frequently leading to systemic inflammatory response syndrome (SIRS), organ damage and multiple-organ dysfunction [1]. The mechanism of pathogenesis of SIRS in the field of hemorrhagic shock is complex and a variety of mechanisms are implicated. The most widely recognized mechanisms are ischemia and reperfusion and stimulation of cells of the innate immune system [2]. Ischemia and reperfusion is mainly participating in oxidative s
Decrease of CD4-lymphocytes and apoptosis of CD14-monocytes are characteristic alterations in sepsis caused by ventilator-associated pneumonia: results from an observational study
Aimilia Pelekanou, Iraklis Tsangaris, Antigoni Kotsaki, Vassiliki Karagianni, Helen Giamarellou, Apostolos Armaganidis, Evangelos J Giamarellos-Bourboulis
Critical Care , 2009, DOI: 10.1186/cc8148
Abstract: Peripheral venous blood was sampled from 68 patients with sepsis within 24 hours of diagnosis; 36 suffered from VAP; 32 from other nosocomial infections, all well-matched for severity, age and sex. Blood monocytes were isolated and cultured with/without purified endotoxin (lipopolysaccharide (LPS)). Estimation of tumour necrosis factor alpha (TNFα) and interleukin-6 (IL-6) in cultures' supernatants was done by an enzyme immunoassay. Flow cytometry was used to determine subpopulations of mononuclear cells and apoptosis. To mimic pathogenesis of VAP, mononuclear cells of healthy volunteers were progressively stimulated with increased inocula of pathogens; apoptosis was determined.In patients with VAP, the absolute number of CD3(+)/CD4(+) lymphocytes was significantly lower (P = 0.034) and apoptosis of isolated monocytes was increased (P = 0.007) compared to other infections. TNFα and IL-6 production from LPS-stimulated monocytes was lower in patients with VAP-related sepsis than with sepsis due to other infections. Apoptosis of monocytes was induced after in vitro stimulation of mononuclear cells by a mechanism mimicking VAP.Decrease of CD4-lymphocytes and immunoparalysis of monocytes are characteristic alterations of sepsis arising in the field of VAP.Sepsis is an important cause of admission and mortality in intensive care units (ICU). In Europe, the Sepsis Occurrence in Acutely Ill Patients study disclosed an ICU mortality rate from sepsis ranging between 27% and 54% depending on the severity [1]. In the USA, 215,000 deaths are reported annually due to sepsis [2].Ventilator associated pneumonia (VAP) is the most common nosocomial infection and the leading cause of sepsis in the ICU. Up to 28% of patients receiving mechanical ventilation will eventually develop VAP, with a mortality rate of up to 70% [3-7].Various explanations have been proposed for the increased mortality of patients with VAP. One previous study from our group in a cohort of 90 patients with sepsis
Immunomodulatory intervention in sepsis by multidrug-resistant Pseudomonas aeruginosa with thalidomide: an experimental study
Evangelos J Giamarellos-Bourboulis, Nikolaos Bolanos, George Laoutaris, Vassilios Papadakis, Vassilios Koussoulas, Despina Perrea, Panayotis E Karayannacos, Helen Giamarellou
BMC Infectious Diseases , 2005, DOI: 10.1186/1471-2334-5-51
Abstract: Sepsis was induced by the intraperitoneal injection of 1 × 108 cfu/kg inoculum of the test isolate in a total of 109 Wistar rats divided in three groups as follows: group A controls; group B administered seed oil 30 minutes before bacterial challenge; and group C administered 50 mg/kg of thalidomide diluted in seed oil 30 minutes before bacterial challenge. Blood was sampled for estimation of endotoxins (LPS), TNFα, interferon-gamma (IFNγ), nitric oxide (NO) and malondialdehyde (MDA). LPS was measured by the QCL-1000 LAL assay, TNFα and IFNγ by ELISA, NO by a colorimetric assay and MDA by the thiobarbiturate assay.Mean (± SE) survival of groups A, B and C were 18.60 ± 1.84, 12.60 ± 0.60 and 30.50 ± 6.62 hours (p of comparisons A to C equal to 0.043 and B to C equal to 0.002). Decreased TNFα and NO levels were found in sera of animals of group C compared to group A. Plasma levels of LPS, MDA and IFNγ did not differ between groups.Intake of thalidomide considerably prolonged survival in experimental sepsis by MDR P.aeruginosa an effect probably attributed to decrease of serum TNFα.Nosocomial infections are commonly caused by multidrug-resistant Gram-negative pathogens. Management of these infections is difficult due to the lack of potent antimicrobial agents; thus a target for immunomodulatory intervention is created [1]. Thalidomide is an old regimen that has been proved potent in reducing the half-life of mRNA of the gene of tumour necrosis factor-alpha (TNFα) in human monocytes [2]. Its anti-angiogenic and anti-TNFα properties have led to its application for the treatment of erythema nodosum leprosum, of cutaneous lupus erythematosus, of Beh?et's syndrome, of multiple myeloma and of HIV-related aphthous ulcers and wasting syndrome [3,4].In a model of experimental sepsis by Escherichia coli, thalidomide was proved very effective in reducing serum levels of TNFα, a phenomenon that was associated with refraining of evolution to sepsis [5]. However, its effect on survi
Diagnostic value of triggering receptor expressed on myeloid cells-1 and C-reactive protein for patients with lung infiltrates: an observational study
Ilias Porfyridis, Diamantis Plachouras, Vasiliki Karagianni, Anastasia Kotanidou, Spyridon A Papiris, Helen Giamarellou, Evangelos J Giamarellos-Bourboulis
BMC Infectious Diseases , 2010, DOI: 10.1186/1471-2334-10-286
Abstract: 68 patients admitted to a medical ward with acute respiratory illness were enrolled in the study. Neutrophil and monocyte TREM-1 expression were measured by flow cytometry, sTREM-1 by an enzyme immunoassay and C-reactive protein by nephelometry. Clinical pulmonary infection score was recorded.34 patients were diagnosed with bacterial community acquired pneumonia (group A) and 34 with non-bacterial pulmonary disease (group B). Median serum TREM-1 concentration was 102.09 pg/ml in group A and lower than 15.10 pg/ml (p < 0.0001) in group B. Mean±SE neutrophil TREM-1 expression was 4.67 ± 0.53 MFI in group A and 2.64 ± 0.25 MFI (p = 0.001) in group B. Monocyte TREM-1 expression was 4.2 ± 0.42 MFI in group A and 2.64 ± 0.35 MFI (p = 0.007) in group B and mean±SE CRP was 18.03 ± 2 mg/ml in group A and 7.1 ± 1.54 mg/ml (p < 0.001) in group B. A cut-off of 19.53 pg/ml of sTREM-1 with sensitivity 82.6% and specificity 63% to discriminate between infectious and non-infectious pulmonary infiltrates was found. sTREM-1 at admission greater than 180 pg/ml was accompanied with unfavourable outcome.TREM-1 myeloid expression and sTREM-1 are reliable markers of bacterial infection among patients with pulmonary infiltrates; sTREM-1 is a predictor of final outcome.Early diagnosis of lung infections remains a challenge. There is no gold standard for diagnosing microbial infection as clinical and laboratory signs are neither sensitive nor specific enough, and microbiological studies often remain negative. The presence of a new infiltrate on plain chest radiograph is considered indicative for diagnosing pneumonia, especially when is supported by clinical and laboratory findings. However it is difficult to differentiate a chest infiltrate of bacterial origin from a chest infiltrate of non-bacterial origin solely based on radiological criteria [1]. The diagnosis of infection is not always clear in the acute setting in patients with respiratory tract disease and a surrogate marker of infecti
Skin Biopsy is Predictive of Outcome in Experimental Sepsis by Multidrug- Resistant Pseudomonas aeruginosa
Pseudomonas aeruginosaVassiliki Tziortzioti, Haritini Petropoulou, Thomas Tsaganos, Aikaterini Spyridaki, Maria Raftogiannis, Evangelos J. Giamarellos-Bourboulis,Nicolaos G. StavrianeasPseudomonas aeruginosa
The Open Dermatology Journal , 2007, DOI: 10.2174/1874372200701010001]
Abstract: To evaluate whether histological findings of skin in sepsis by Pseudomonas aeruginosa could be a predictive factor of progression to death, histological alterations after challenge by one multidrug-resistant isolate were studied in 24 rabbits. Acute pyelonephritis was induced after ligation of the right ureter and injection of 108 CFU per kg of body weight into the renal pelvis. Biopsy samples of skin were taken on necropsy. Mean survival of animals after bacterial challenge was 5.23 days. Main histological findings of skin were inflammation and swelling of dermis; thickening of endothelium; presence of thrombi in vessels; necrobiotic changes of the hair follicles. Serum TNFα was negatively correlated to histology of dermis and follicles. Positive correlation was found between survival and swelling of dermis. It is concluded that prolongation of survival was accompanied by intense edema of the dermis. A punch skin biopsy might be a predictive factor of sepsis outcome.
Compartmentalization of lipid peroxidation in sepsis by multidrug-resistant gram-negative bacteria: experimental and clinical evidence
Chryssoula Toufekoula, Vassileios Papadakis, Thomas Tsaganos, Christina Routsi, Stylianos E Orfanos, Anastasia Kotanidou, Dionyssia-Pinelopi Carrer, Maria Raftogiannis, Fotini Baziaka, Evangelos J Giamarellos-Bourboulis
Critical Care , 2013, DOI: 10.1186/cc11930
Abstract: Lethal sepsis was induced in rats by the intraperitoneal injection of one MDR isolate of Pseudomonas aeruginosa. Produced malondialdehyde (MDA) was measured in tissues 5 hours after bacterial challenge with the thiobarbiturate assay followed by high-performance liquid chromatography (HPLC) analysis. Results were compared with those from a cohort of patients with ventilator-associated pneumonia (VAP) and sepsis by MDR Gram-negative bacteria. More precisely, serum MDA was measured on 7 consecutive days, and it was correlated with clinical characteristics.MDA of septic rats was greater in the liver, spleen, and aortic wall, and it was lower in the right kidney compared with sham operated-on animals. Findings were confirmed by the studied cohort. Circulating MDA was greater in patients with hepatic dysfunction and acute respiratory distress syndrome (ARDS) compared with patients without any organ failures. The opposite was found for patients with acute renal dysfunction. No differences were found between patients with ARDS without or with cardiovascular (CV) failure and patients without any organ failure. Serial measurements of MDA in serum of patients indicated that levels of MDA were greater in survivors of hepatic dysfunction and ARDS and lower in survivors of acute renal dysfunction.Animal findings and results of human sepsis are complementary, and they suggest a compartmentalization of lipid peroxidation in systemic infections by MDR gram-negative bacteria.Oxidative stress results from an imbalance between production of reactive oxygen and nitrogen species (ROS and RNS) and endogenous antioxidant defense mechanisms [1]. A growing body of evidence suggests that many of the effects of cellular dysfunction under oxidative stress are mediated by products of nonenzymatic reactions, such as the peroxidative degradation of polyunsaturated fatty acids. Aldehyde molecules generated during lipid peroxidation are considered ultimate mediators of toxic effects elicited by oxid
Early apoptosis of blood monocytes in the septic host: is it a mechanism of protection in the event of septic shock?
Evangelos J Giamarellos-Bourboulis, Christina Routsi, Diamantis Plachouras, Vassiliki Markaki, Maria Raftogiannis, Dimitrios Zervakis, Vassilios Koussoulas, Stylianos Orfanos, Anastasia Kotanidou, Apostolos Armaganidis, Charis Roussos, Helen Giamarellou
Critical Care , 2006, DOI: 10.1186/cc4921
Abstract: Blood monocytes were isolated from 90 patients with septic syndrome due to ventilator-associated pneumonia on days 1, 3, 5 and 7 from the initiation of symptoms. Apoptosis was defined after incubation with annexin-V-fluorescein isothiocyanate and propidium iodine and reading by a flow cytometer. The function of first-day monocytes was evaluated from the concentrations of tumour necrosis factor alpha (TNFα) and IL-6 in supernatants of cell cultures after triggering with endotoxins. TNFα, IL-6 and IL-8 were estimated in serum by an enzyme immunoassay.Mortality rates of patients with apoptosis ≤50% compared with patients with apoptosis >50% were 49.12% and 15.15%, respectively (P < 0.0001). Kaplan-Meier analysis showed a 28-day survival benefit in patients with septic shock and monocyte apoptosis >50% compared with those patients with apoptosis ≤50% (P = 0.0032). Production of IL-6 by monocytes on the first day by patients with apoptosis ≤50% was similar compared with monocytes isolated from healthy controls. Serum concentrations of TNFα were higher in patients with monocyte apoptosis ≤50% and septic shock compared with patients with apoptosis >50% on day 7; similar findings occurred for serum IL-6 on days 1 and 7 and for serum IL-8 on days 1 and 5.Early apoptosis of monocytes upon presentation of clinical signs of sepsis is connected to a favourable outcome. These findings are of particular importance for the patient with septic shock, where they might constitute a mechanism of pathogenesis.Apoptotic cascade is a process already described to supervene during the evolution of sepsis in lymphocytes, in tissue macrophages and in intestinal epithelia, and it is connected to organ dysfunction [1]. Although data for the apoptosis of cells of the adaptive immune system are available, little evidence exists for the implication of the innate immune system [2]. The need for knowledge in that field is further aggravated by the central role of monocytes in the pathogenesis of sep
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