The Evaluation of the Role of the Cytokines TNF- alfa and IL 6 in the Production of Hypoalbuminemia in Patients Undergoing Major Surgical Interventions

2018 ◽  
Vol 69 (7) ◽  
pp. 1830-1837
Author(s):  
Cristian Nicolescu ◽  
Alaxendru Pop ◽  
Alin Mihu ◽  
Luminita Pilat ◽  
Ovidiu Bedreag ◽  
...  
Keyword(s):  
Surgical Procedure ◽  
Tnf Alpha ◽  
Phase Reaction ◽  
Statistical Validation ◽  
Necrosis Factor Alpha ◽  
Surgical Interventions ◽  
Plasmatic Level ◽  
Factor Alpha ◽  
Validation Tests

This article presents an observational randomized prospective study done on 65 patients, who underwent major surgical interventions in the field of orthopedic surgery-total hip replacement or general surgery � total colectomy. The level of albuminemia in these cases were determined before the surgical intervention, after 6 hours of the intervention and after 24 h of the intervention. The measurements of the plasmatic concentration of the pro-inflammatory cytokines Tumor Necrosis factor -alpha (TNF-alpha) and interleukin 6 (IL6) were simultaneously done with the determination of the plasmatic levels of albumin. Values of hemoglobin and hematocrit were determined 24 h after the surgical procedure in order to exclude hemodilution, which could lead to a possible drop in the levels of plasmatic albumin. After the collection of the data, the statistical work was done and it consisted of descriptive statistics, correlation and comparison tests as well as statistical validation tests. Obtained results indicate that IL-6 plays a major role comparatively with that of TNF-alfa, regarding the decrease of the plasmatic level of albumin, and due to this, the primordial cause for hypoalbuminemia is an acute hepatic phase reaction. Supplemental permeability of the capillary wall under the action of TNF alpha has a secondary role, but could lead to a faster decrease in plasmatic albumin in the first hours after the surgical procedure.

Comparison between effects of interleukin-1 alpha administration and sublethal endotoxemia in primates

1991 ◽  
Vol 261 (2) ◽  
pp. R442-R452 ◽  
Author(s):  
E. Fischer ◽  
M. A. Marano ◽  
A. E. Barber ◽  
A. Hudson ◽  
K. Lee ◽  
...  
Keyword(s):  
Adrenocorticotropic Hormone ◽  
Interleukin 1 ◽  
Tnf Alpha ◽  
Phase Reaction ◽  
Necrosis Factor Alpha ◽  
Hormonal Responses ◽  
Alpha Response ◽  
Factor Alpha ◽  
Dose Dependent ◽  
Necrosis Factor

Interleukin (IL)-1 is an early mediator of host response to inflammation, although its contribution to individual components of the acute phase reaction is still unclear. To evaluate how the hemodynamic, metabolic, and hormonal responses to sublethal endotoxemia compare with IL-1 administration, baboons received intravenously either lipopolysaccharide (LPS) or 0.1, 10, or 100 micrograms/kg IL-1 alpha. LPS induced an early tachycardia and a fall in mean arterial pressure, as well as lacticacidemia and hypoaminoacidemia. Similar hemodynamic and metabolic changes were seen with 10 or 100 micrograms/kg of IL-1 alpha. An increase in adrenocorticotropic hormone and fall in serum iron were induced by IL-1 alpha but not by LPS. Plasma tumor necrosis factor-alpha (TNF-alpha) was not measurable after IL-1 alpha administration, whereas LPS induced a monophasic TNF-alpha response. IL-6 levels were significantly greater after LPS than IL-1 alpha administration. Histopathological lesions, similar in LPS- and 100 micrograms/kg IL-1 alpha-treated groups, were present only in the adrenal cortex. We conclude that many, but not all, of the effects of sublethal endotoxemia can be replicated by IL-1 alpha administration, and these responses are dose dependent.

scholarly journals Possible Alterations in the Plasma Levels of Pro (TNF-alpha) and Anti-inflammatory (IL-10) Cytokines in Long-Term Insomnia

2019 ◽  
Vol 5 ◽  
pp. 1
Author(s):  
Mathew F. Olaniyan ◽  
Alade Ogunlade ◽  
◽  
Keyword(s):  
Chronic Insomnia ◽  
Tnf Alpha ◽  
Infectious Agents ◽  
Necrosis Factor Alpha ◽  
Significant Difference ◽  
Before And After ◽  
Factor Alpha ◽  
Microbial Agents

Long-term/chronic insomnia occurs in patients for over one month; it can affect the functions of the immune system and responses, which may involve cytokines. The aim was to determine alterations of Tumor necrosis factor alpha (TNF-alpha) and IL-10 cytokines in long-term insomnia. Thirty-three long-term/chronic insomnia patients (male, 22; female, 11) aged 47-61 years were initially recruited. Seven of them who were infected with microbial agents were excluded from the study. Of the 26 free of infectious agents only 21 (female, 5; male, 16) were successfully monitored. Age-matched apparently healthy non-insomnia subjects (male, 25; female, 25) free of the infectious agents were recruited as control. Plasma TNF-alpha, IL-10, HBsAg, anti-HCV, and HIVp24 antigen were assayed by ELISA method while determination of Mycobacterium tuberculosis was by Ziehl–Neelsen staining of sputum and Plasmodium spp. by thick blood Giemsa staining. Of the 33 insomnia patients initially recruited, 21.2% (7) were infected with microbial agents (Plasmodium spp., 6.1% (2); HCV, 3.0% (1); HBV, 6.1% (2); Mycobacterium tuberculosis, 3.0% (1); Plasmodium spp. + HBV, 3.0% (1); and HIVp24, 0). Twenty-one chronic insomnia patients were finally investigated on cytokines. There were significantly higher mean plasma values of TNF-alpha and IL-10 cytokines in chronic insomnia patients before treatment than the values obtained in the control subjects (p < 0.05). The results also showed a significantly lower mean plasma value of TNF-alpha cytokine in chronic insomnia patients after treatment than the values obtained in the patients before treatment. There were no significant differences in the mean plasma values of IL-10 cytokines in chronic insomnia patients before and after treatment (p > 0.05). There was a significant increase in plasma TNF-alpha and IL-10 cytokines in long-term insomnia patients before treatment while plasma TNF-alpha significantly decreased after treatment, and no significant difference was obtained in the plasma IL-10 before and after treatment. TNF-alpha could be a good investigative index of insomnia.

scholarly journals Tumour necrosis factor-alpha concentration in severely asthmatic children

2000 ◽  
Vol 6 (2-3) ◽  
pp. 432-436
Author(s):  
M. N. Massoud
Keyword(s):  
Severe Asthma ◽  
Late Phase ◽  
Tumour Necrosis Factor Alpha ◽  
Tnf Alpha ◽  
Phase Reaction ◽  
Necrosis Factor Alpha ◽  
Asthmatic Children ◽  
Late Phase Reaction ◽  
Factor Alpha ◽  
Necrosis Factor

We assessed tumour necrosis factor-alpha [TNF-alpha] concentrations in 80 asthmatic children, 26 with severe asthma in early-phase reaction, 26 with severe asthma in late-phase reaction, 28 with severe asthma controlled in between attacks with oral prednisone and 20 matched control children. TNF-alpha was measured in patients’ plasma and in a supernatant of lipopolysaccharide-stimulated [LPS]peripheral blood mononuclear [PBM] cells. TNF-alpha concentrations in plasma and the supernatant of LPS-stimulated cells were positively correlated and the concentration also correlated positively with the time lapse between the start of the asthma attack and the time of blood sampling. TNF-alpha concentration was significantly higher in the late-phase reaction group compared to the other groups, indicating a need to counteract its release and/or effects early in asthma patients

Leukogram and cortisol parameters in Swiss mice experimentally infected with Angiostrongylus costaricensis

2021 ◽  
Vol 95 ◽  
Author(s):  
E. Benvegnú ◽  
C.C. Hermes ◽  
J.A. Guizzo ◽  
S.M. Soares ◽  
M.M. Costa ◽  
...  
Keyword(s):  
Cytokine Profile ◽  
Control Group ◽  
Necrosis Factor Alpha ◽  
Swiss Mice ◽  
Hypochromic Anaemia ◽  
Third Stage ◽  
Factor Alpha ◽  
Cortisol Levels ◽  
Necrosis Factor

Abstract This study describes changes in haematological parameters, cytokine profile, histopathology and cortisol levels in Swiss mice experimentally infected with Angiostrongylus costaricensis. Twenty-eight Swiss mice were divided into two groups (G1 and G2) of 14 animals each. In each group, eight animals were infected orally with ten third-stage larvae of A. costaricensis and six were used as a control group. The mice of groups G1 and G2 were sacrificed 14 and 24 days after infection, respectively. Samples were collected for histopathological and haematological analyses and determination of the cytokine profile and cortisol levels. Granulomatous reaction, eosinophilic infiltrate and vasculitis in the intestinal tract, pancreas, liver and spleen were observed with varying intensity in infected animals. Our results showed that the mice developed normocytic and hypochromic anaemia, and that the histopathological lesions caused by the experimental infection influenced increases in cortisol, neutrophil and monocyte levels. In addition to this, we detected increased interleukin-6 and tumour necrosis factor alpha levels in the infected animals.

Tumor necrosis factor-alpha inhibits lipid and lipoprotein transport by Caco-2 cells

1995 ◽  
Vol 269 (6) ◽  
pp. G953-G960 ◽  
Author(s):  
M. Mehran ◽  
E. Seidman ◽  
R. Marchand ◽  
C. Gurbindo ◽  
E. Levy
Keyword(s):  
Lipid Metabolism ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Low Density Lipoproteins ◽  
Tnf Alpha ◽  
Low Density ◽  
Necrosis Factor Alpha ◽  
Apo B ◽  
Factor Alpha ◽  
Necrosis Factor

Cytokines, important mediators of inflammation, have been shown to cause disturbances in circulating and hepatic lipid metabolism. Although the intestine plays a major role in dietary fat transport and largely contributes to plasma lipoproteins, the effects of cytokines on intestinal lipid handling remain unknown. In the present study, the modulation of lipid, apoprotein, and lipoprotein synthesis and secretion by tumor necrosis factor-alpha (TNF-alpha) was investigated in Caco-2 cells. Highly differentiated and polarized cells (20 days in culture) were incubated for 20 h with recombinant human TNF-alpha (100-500 ng/ml). No cytotoxic effect of TNF-alpha cells was observed, as indicated by the determinations of Caco-2 cell viability and monolayer transepithelial resistance. Moreover, no differences in cell maturation (sucrase activity) or cell proliferation ([3H]thymidine incorporation and cell cycle analysis) were detected between treated and control cultures. Significant inhibition of lipid secretion by TNF-alpha was observed, with the greatest reduction at 500 ng/ml. TNF-alpha significantly decreased Caco-2 cell secretion of phospholipids (22%), triglycerides (30%), and cholesteryl ester (37%). It also significantly diminished the export of newly synthesized low-density lipoproteins (LDL; 20%) and high-density lipoproteins (HDL; 13%), with a lesser effect on very low-density lipoproteins (VLDL; 3%). The lipid composition of these lipoproteins was minimally affected. De novo synthesis of apo A-I, apo B-100, and apo B-48 was also markedly reduced by TNF-alpha. Sphingomyelinase activity was not increased and cell content of sphingomyelin was not altered, suggesting that inhibitory effects on lipid and apoprotein of TNF-alpha were not mediated by the ceramide pathway. Our results indicate that TNF-alpha may play a role in modulating intestinal lipid metabolism, thus affecting circulating lipoproteins.

scholarly journals Lipopolysaccharides prime whole human blood and isolated neutrophils for the increased synthesis of 5-lipoxygenase products by enhancing arachidonic acid availability: involvement of the CD14 antigen.

1993 ◽  
Vol 178 (4) ◽  
pp. 1347-1355 ◽  
Author(s):  
M E Surette ◽  
R Palmantier ◽  
J Gosselin ◽  
P Borgeat
Keyword(s):  
Arachidonic Acid ◽  
Mononuclear Cells ◽  
Leukotriene B4 ◽  
Eicosatetraenoic Acid ◽  
Tnf Alpha ◽  
Peripheral Blood Mononuclear ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Priming Activity

Stimulation of heparinized blood with 1 microM formyl-methionyl-leucyl-phenylalanine (FMLP) resulted in the formation of &lt; 30 pmol/ml plasma of 5-lipoxygenase (5-LO) products. The preincubation of blood with 1 microgram/ml of lipopolysaccharide (LPS) (Escherichia coli 0111-B4) for 30 min before stimulation with FMLP resulted in the accumulation of 250-300 pmol of 5-LO products per ml plasma. The major products detected were leukotriene B4 and (5S)-hydroxy-6,8,11,14-eicosatetraenoic acid which were produced in equivalent amounts. The priming activity was detectable with as little as 1-10 ng LPS per ml blood and was optimal using 1-10 micrograms LPS/ml blood. The priming for 5-LO product synthesis was optimal after 20-30 min of preincubation with LPS and declined at preincubation times &gt; 30 min. The priming effect of LPS was also observed using the complement fragment C5a or interleukin 8 as agonists. Polymorphonuclear leukocytes (PMN) and peripheral blood mononuclear cells accounted for 80 and 20% of the synthesis of 5-LO products, respectively. The ability of LPS to prime isolated PMN was dependent on the presence of plasma and was inhibited by the anti-CD14 antibody IOM2, indicating a CD14-dependent priming mechanism. The priming of whole blood with tumor necrosis factor alpha (TNF-alpha) and LPS was additive and the presence of mononuclear cells did not enhance the ability of LPS to prime PMN, indicating that the priming activity of LPS is independent of LPS-induced TNF-alpha synthesis. The mechanism by which LPS enhance 5-LO product synthesis in PMN was investigated. Treatment of PMN with LPS strongly enhanced the release of arachidonic acid after stimulation with FMLP. The release of arachidonic acid was optimal 2-3 min after stimulation with FMLP, attaining levels 5-15-fold greater than those observed in unprimed cells stimulated with FMLP. These results demonstrate that LPS dramatically increases the ability of blood to generate 5-LO products, and support the putative role of leukotrienes in pathological states involving LPS.

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