Higher Plasma Levels Of TNF-alpha Research Articles

Plasma Levels of TNF-αl and IL-10 in Plasmodium falciparum co-infection with Mycobacterium tuberculosis

NTFα is a proinflammatory cytokine which acts to worsen disease while IL-10 is an anti-inflammatory cytokine, which acts to improve healing. Plasmodium falciparum co-infection with Mycobacterium tuberculosis could generate both innate and acquired immunity involving inflammatory responses. This work was designed to determine plasma level of TNF-Alpha and IL-10 in plasmodium co-infection with Mycobacterium tuberculosis . The test subjects recruited for this study were M. tuberculosis mono-infected patients (30), Plasmodium falciparum mono-infected patients (50) and M. tuberculosis and plasmodium coinfected patients (30) aged 32-73years. M. tuberculosis and plasmodium non-infected subjects (50) were studied as control. All subjects were seronegative to HIV, HCV and HBsAg. TNF-Alpha, IL-10, HIV, HCV and HBsAg were determined in each of the subjects by immunochemical technique using ELISA method. M. tuberculosis was identify in each of the subjects by fluorescence microscopy and sputum culture on Lowenstein–Jensen medium while identification of plasmodium was carried out using thick and thin film technique using Geimsha and leishman staining. The result obtained showed a significantly higher plasma levels of TNF-alpha and IL-10 in patients who were co-infected with both plasmodium and M. tuberculosis compared with Plasmodium falciparum mono—infected, M. tuberculosis mono-infected patients and also compared with the control subjects (p<0.05). This work reveals a significant increase in plasma value of TNF-alpha and IL-10 in M. tuberculosis and plasmodium co-infections compared with either plasmodium or M.tuberculosis mono-infections. Routine laboratory evaluation of these parameters in M. tuberculosis and plasmodium co-infection will provide useful direction for the management of the disease condition. Keywords: , NTFα IL-10, plasmodium co-infection, Mycobacterium tuberculosis

Age may determine the effect of hypolipidemic agents on plasma adipokine levels in patients with elevated low-density lipoprotein cholesterol levels.

Lipid-lowering agents affect adipose tissue function. No study has investigated the role of age in the effects of hypolipidaemic agents on plasma adipokines. The study was a retrospective analysis of data of 65 hypercholesterolaemic patients treated for 90 days with simvastatin, ezetimibe, or simvastatin/ezetimibe combination therapy. Circulating levels of leptin, adiponectin, visfatin, and tumour necrosis factor alpha (TNF-alpha), as well as high-sensitivity C-reactive protein (hsCRP) were assessed separately for patients aged between 35 and 50 years and between 51 and 65 years, at the beginning and at the end of treatment. Patients in the age between 51 and 65 years had higher plasma levels of TNF-alpha and hsCRP, and lower plasma levels of adiponectin than patients aged between 35 and 50 years. In both age groups, simvastatin reduced plasma levels of hsCRP, leptin, visfatin, and TNF-alpha and increased circulating levels of adiponectin. This effect was particularly pronounced if simvastatin was administered in combination with ezetimibe. Ezetimibe alone increased plasma adiponectin and reduced plasma levels of leptin and hsCRP only in older adults. Irrespectively of age, ezetimibe administered alone did not affect visfatin and TNF-alpha. The effect of simvastatin on plasma hsCRP and the investigated adipokines did not differ between both groups. In turn, the effect of ezetimibe and simvastatin/ezetimibe combination therapy on leptin, adiponectin, and hsCRP was stronger in older than in younger adults. Our results show that age may partially determine the effect of ezetimibe, but not of simvastatin, on adipose tissue function. (Endokrynol Pol 2016; 67 (3): 271-276).

Circulating levels of TNF-α and its soluble receptors in the plasma of patients with epithelial ovarian cancer

The significance of circulating levels of TNF-alpha and its soluble receptors (sTNF-Rs) in the plasma of patients with epithelial ovarian cancer (EOC) has not been fully elucidated. The present study was to investigate the relationship of pretreatment plasma levels of TNF-alpha, sTNFR-1 and sTNFR-2 with outcome in 126 patients with EOC. Concentrations of TNF-alpha and sTNF-Rs were determined by enzyme-linked immunosorbent assay (ELISA). Median TNF-alpha and sTNF-Rs levels were significantly higher in EOC patients than in healthy controls. High plasma levels of TNF-alpha and sTNF-Rs were correlated with tumor stage and with reduced mean survival time (MST). The results of the present study suggested that preoperative plasma TNF-alpha and sTNF-Rs levels in EOC patients correlated with the highest risk of cancer progression. Thus, the clinical value of an activated TNF system in EOC needs to be further investigated.

TREATMENT WITH THE GLYCOGEN SYNTHASE KINASE-3β INHIBITOR, TDZD-8, AFFECTS TRANSIENT CEREBRAL ISCHEMIA/REPERFUSION INJURY IN THE RAT HIPPOCAMPUS

The serine/threonine glycogen synthase kinase 3beta (GSK-3beta) is abundant in the central nervous system, particularly in the hippocampus, and plays a pivotal role in the pathophysiology of a number of diseases, including neurodegeneration. This study was designed to investigate the effects of GSK-3beta inhibition against I/R injury in the rat hippocampus. Transient cerebral ischemia (30 min) followed by 1 h of reperfusion significantly increased generation of reactive oxygen species and modulated superoxide dismutase activity; 24 h of reperfusion evoked apoptosis (determined as mitochondrial cytochrome c release and Bcl-2 and caspase-9 expression), resulted in high plasma levels of TNF-alpha and increased expression of cyclooxygenase-2, inducible nitric oxide synthase, and intercellular adhesion molecule-1. The selective GSK-3beta inhibitor, 4-benzyl-2-methyl-1,2,4-thiadiazolidine-3,5-dione (TDZD-8), was administered before and after ischemia or during reperfusion alone to assess its potential as prophylactic or therapeutic strategy. Prophylactic or therapeutic administration of TDZD-8 caused the phosphorylation (Ser(9)) and hence inactivation of GSK-3beta. Infarct volume and levels of S100B protein, a marker of cerebral injury, were reduced by TDZD-8. This was associated with a significant reduction in markers of oxidative stress, apoptosis, and the inflammatory response resulting from cerebral I/R. These beneficial effects were associated with a reduction of I/R-induced activation of the mitogen-activated protein kinases JNK1/2 and p38 and nuclear factor-kappaB. The present study demonstrates that TDZD-8 protects the brain against I/R injury by inhibiting GSK-3beta activity. Collectively, our data may contribute to focus the role of GSK-3beta in cerebral I/R.

Tumor Necrosis Factor Alpha Influences the Inflammatory Response After Coronary Surgery

A systemic inflammatory response is not uncommonly observed after coronary revascularization. Tumor necrosis factor alpha is one of a number of modulators of this response. A functional polymorphism within the TNFalpha gene at position G-308A has been associated with increased TNFalpha levels. The relationship between predicted TNFalpha genotype and circulating TNFalpha levels in patients undergoing coronary revascularization surgery has yet to be defined. We examined the relationship between TNFalpha G-308A polymorphism, TNFalpha postoperative levels, and clinical outcome after coronary revascularization surgery. We obtained DNA from 96 consecutive patients who underwent elective coronary revascularization. Patients were genotyped for TNFalpha G-308A polymorphism using sequence specific primer-polymerase chain reaction (SSP-PCR). Tumor necrosis factor alpha levels were measured on serum samples taken 3 hours postoperatively using enzyme-linked immunosorbent assay (ELISA). The prevalence of AA, AG, and GG TNFalpha-308 genotype was 12%, 40%, and 48%, respectively. Patients homozygous for A had higher circulating levels of TNFalpha (p = 0.009). Higher levels of TNFalpha were significantly associated with prolonged intensive care unit stay (p = 0.008), increase usage of an inotropic agent (p = 0.024), increased mortality risk (p = 0.018), and diabetes (p = 0.019). These remained statistically significant after risk stratification. Patients of the AA-308 TNFalpha genotype showed significantly higher TNFalpha plasma levels. Higher plasma levels of TNFalpha were associated with less favorable outcome after coronary revascularization surgery. It may prove useful to utilize TNFalpha serum levels as a marker for identifying high-risk patients in the future.

Systemic Inflammatory Markers, Periodontal Diseases, and Periodontal Infections in an Elderly Population

To study the levels of systemic markers for inflammation with parameters of periodontal diseases in older people. A cross-sectional study was conducted in a cohort that is being followed prospectively on the effects of aging and body composition on morbidity. University of Pittsburgh, Pittsburgh, and University of Tennessee, Memphis. One thousand one hundred thirty-one participants (mean age+/-standard deviation 72.7+/-2.8); 66% white and 50% male. Periodontal examination, including probing depth and attachment loss, was performed. Periodontal disease extent was divided into 0% of sites with probing depth of 6 mm or more, 1% to 10% of sites with probing depth of 6 mm or more and more than 10% of sites with probing depth of 6 mm or more. Subgingival plaque samples were collected from four molar teeth, and the levels of periodontal pathogens were determined using the benzoyl-DL-arginine-naphthylamide (BANA) test. Plasma interleukin-6 (IL-6), C-reactive protein (CRP), plasminogen activator inhibitor type-1 (PAI-1), and tumor necrosis factor alpha (TNF-alpha) levels were measured in all participants. Assessments of risk factors associated with elevated levels of markers of systemic inflammation were also determined. Multiple regression analysis was employed to analyze the data. IL-6 levels were significantly higher in participants with more-extensive periodontal disease than in other participants. Periodontal disease extent was significantly associated with higher TNF-alpha plasma levels, controlling for established risk factors for elevated TNF-alpha levels. Participants with BANA-positive species had significantly higher CRP plasma levels when controlling for risk factors for elevated CRP levels. Periodontal disease and infection may be modifiable risk indicators for elevated levels of systemic inflammatory markers in older people.

Prostacyclin inhibition by indomethacin aggravates hepatic damage and encephalopathy in rats with thioacetamide-induced fulminant hepatic failure

Vasodilatation and increased capillary permeability have been proposed to be involved in the pathogenesis of acute and chronic form of hepatic encephalopathy. Prostacyclin (PGI2) and nitric oxide (NO) are important contributors to hyperdynamic circulation in portal hypertensive states. Our previous study showed that chronic inhibition of NO had detrimental effects on the severity of encephalopathy in thioacetamide (TAA)-treated rats due to aggravation of liver damage. To date, there are no detailed data concerning the effects of PGI2 inhibition on the severity of hepatic encephalopathy during fulminant hepatic failure. Male Sprague-Dawley rats weighing 300-350 g were used. Fulminant hepatic failure was induced by intraperitoneal injection of TAA (350 mg/(kg.d) for 3 d. Rats were divided into two groups to receive intraperitoneal injection of indomethacin (5 mg/(kg.d), n = 20) or normal saline (N/S, n = 20) for 5 d, starting 2 d before TAA administration. Severity of encephalopathy was assessed by the counts of motor activity measured with Opto-Varimex animal activity meter. Plasma tumor necrosis factor-alpha (TNF-alpha, an index of liver injury) and 6-keto-PGF(1alpha) (a metabolite of PGI2) levels were measured by enzyme-linked immunosorbent assay. As compared with N/S-treated rats, the mortality rate was significantly higher in rats receiving indomethacin (20% vs 5%, P<0.01). Inhibition of PGI2 created detrimental effects on total movement counts (indomethacin vs N/S: 438+/-102 vs 841+/-145 counts/30 min, P<0.05). Rats treated with indomethacin had significant higher plasma levels of TNF-alpha (indomethacin vs N/S: 22+/-5 vs 10+/-1 pg/mL, P<0.05) and lower plasma levels of 6-keto-PGF1alpha (P<0.001), but not total bilirubin or creatinine (P>0.05), as compared with rats treated with N/S. Chronic indomethacin administration has detrimental effects on the severity of encephalopathy in TAA-treated rats and this phenomenon may be attributed to the aggravation of liver injury. This study suggests that PGI2 may provide a protective role in the development of fulminant hepatic failure.

The tumor necrosis factor alpha -308G>A polymorphism is associated with dementia in the oldest old.

To test the hypothesis that the tumor necrosis factor (TNF) -308 G>A promoter gene polymorphism is a risk factor in age-related dementia and longevity. A cross-sectional and a longitudinal study. A population-based sample of Danish centenarians. One hundred-year-old Danes (n=122) from "The Longitudinal Study of Danish Centenarians." Octogenarians (n=174) and healthy volunteers aged 18 to 30 (n=47) served as reference groups. Whether the distribution of TNF -308 GG/GA/AA genotypes were different in centenarians than in younger age groups was investigated (Fischer exact test). Furthermore, whether the TNF -308 G>A polymorphism was associated with the prevalence of dementia (logistic regression analysis), the plasma level of TNF-alpha (analysis of variance), and mortality in the following 5 years (Cox regression analysis) within the cohort of centenarians was tested. The distribution of TNF -308 genotypes was not different across the three different age groups, but the GA genotype was associated with decreased prevalence of dementia in centenarians. The few centenarians with AA carrier status had higher mortality risk and tended to show higher plasma levels of TNF-alpha, but the significance was questionable due to a low number of subjects with this genotype. It is possible that the TNF -308 A allele is maintained during aging because subjects who are heterozygous for this polymorphism possess the optimal inflammatory response with regard to protection against age-related neurodegeneration.

Circulating levels of TNF-alpha and IL-6-relation to truncal fat mass and muscle mass in healthy elderly individuals and in patients with type-2 diabetes

The purpose of the current study was to test the hypothesis that an altered fat distribution in elderly healthy subjects and in patients with type-2 diabetes contributes to high circulating levels of interleukin (IL)-6 and tumor necrotic factor (TNF)-alpha, which secondly is related to lower muscle mass. Twenty young controls, (20–35 yr), 20 healthy elderly subjects (65–80 yr) and 16 elderly patients with type 2 diabetes (65–80 yr) were included in a cross sectional study. Plasma levels of TNF-alpha and IL-6 were measured after an overnight fast. Dual-energy X-ray absorptiometry and total body potassium counting measured truncal fat, appendicular skeletal muscle mass (ASM) and body cell mass (BCM), respectively. TNF-alpha, IL-6 and the relative truncal fat mass were higher in elderly compared with young controls. ASM was lower in diabetic men than in young controls and BCM was lower in elderly men compared with young men. TNF-alpha and IL-6 were correlated with the absolute as well as the relative truncal fat mass in univariate regression analyses. Similar results were found in multivariate linear regression analyses after adjusting for the effect of age and gender. TNF-alpha was related to lower ASM and BCM in elderly men both in a univariate regression analysis and a multivariate regression analysis. In conclusion, high plasma levels of TNF-alpha and IL-6 in elderly healthy people and in patients with type 2 diabetes are associated with increased truncal fat mass, suggesting that cytokines are partly derived from this adipose tissue bed. Furthermore, TNF-alpha was related to lower ASM and BCM, suggesting that TNF-alpha contributes to sarcopenia in ageing.

Age-associated loss of immunomodulatory protection by granulocyte-colony stimulating factor in endotoxic rats.

Elderly patients have a higher incidence of morbidity and mortality due to infectious diseases. Because most immune functions in the elderly differ compared with those in younger subjects, we studied the effect of the immunomodulating agent G-CSF on endotoxic liver injury and cytokine release in an aging animal model of acute sepsis. Young (3-month-old), mature (12-month-old), and senescent (24-month-old) male Sprague-Dawley rats (n = 6 each) were treated with bacterial endotoxin for 6 h. Age-matched groups of animals (n = 6 each) received G-CSF (200 microg/kg i.v.) 1 h prior to endotoxin. LPS-induced hepatic toxicity, as assessed in vivo by nutritive perfusion failure, intravascular leukocyte accumulation, biliary excretion dysfunction, and liver enzyme release, was significantly more pronounced in mature and old animals when compared with young animals. Concomitantly, mature but, in particular, senescent endotoxic animals exhibited 2- to 14-fold higher plasma levels of TNF-alpha, IL-1beta, IL-6, IL-10, and Rantes than young endotoxic rats. The percentage of G-CSF receptor surface expression on neutrophils did not significantly differ between young, mature, and senescent animals (36%-46%) and was found comparably down-regulated at 6 h after LPS exposure (15%-19%). Kupffer cell activation, i.e., clearance of intravascularly applied fluorescent latex beads, did not differ between the LPS-exposed age groups. G-CSF dampened LPS-induced Kupffer cell activation, and significantly reduced plasma cytokine levels in young and mature, but not in senescent animals. Thereby, G-CSF caused attenuation of hepatic tissue injury in all except the senescent endotoxic animals. In summary, our results show an age-dependent increase in hepatic LPS toxicity. Because flow cytometric analysis of G-CSF receptor expression disproved that cytokinemia-induced down-regulation of G-CSF receptors might account for the unresponsiveness to G-CSF in the senescent animals, other homeostatic regulatory mechanisms appear to undergo changes with age that bring out a disrupted balance between inflammatory cytokines with unresponsiveness to G-CSF and, thus, compromised host defense mechanisms in the elderly.

Proinflammatory cytokines, antibodies to Chlamydia pneumoniae and age-associated diseases in Danish centenarians: is there a link?

Plasma levels of tumour necrosis factor (TNF)-alpha levels increase with age. High levels are associated with dementia and atherosclerosis in centenarians. Chlamydia pneumoniae induces the production of proinflammatory cytokines and has been related to the pathogeneses of Alzheimer's disease and cardiovascular diseases. The purpose of this study was to test the hypothesis that circulating levels of TNF-alpha represent a link between C. pneumoniae, high prevalences of dementia and cardiovascular diseases in 126 Danish centenarians. IgA antibody titres against C. pneumoniae were linearly correlated with high plasma levels of TNF-alpha in centenarians. However, both parameters were also correlated with total IgA in the blood and the association between C. pneumoniae IgA and TNF-alpha was not significant when total IgA was included in a multiple linear regression model. Accordingly, the association between C. pneumoniae-specific IgA and TNF-alpha may reflect immune activation rather than a specific antibody response. No associations were found between antibodies to C. pneumoniae and dementia or cardiovascular diseases. Although TNF-alpha is likely to be involved in the pathogenesis of atherosclerosis and dementia, the present study does not support the hypothesis that TNF-alpha represents a link between chronic C. pneumoniae infection and these disorders.

Stimulation of beta-adrenergic receptors inhibits the release of tumor necrosis factor-alpha from the isolated rat heart.

Beta-adrenergic receptor agonists such as isoproterenol inhibit production of tumor necrosis factor (TNF)-alpha in a number of cell types. Because the heart is a source of TNF-alpha, we hypothesized that isoproterenol would inhibit cardiac production of the cytokine. Analysis of cardiac release of TNF-alpha. Medical research laboratory. Rats. None. With the approval of the Institutional Animal Care and Use Committee, rats were anesthetized and hearts were removed and perfused. After 30 mins, bacterial lipopolysaccharide (LPS) with or without isoproterenol was infused for 60 mins. At 30, 60, 90, 120, and 150 mins, coronary flow was measured and coronary effluent was analyzed for TNF-alpha. Cardiac production of TNF-alpha was expressed as pg/min. Cyclic adenosine monophosphate (AMP) in the coronary effluent was measured. TNF-alpha messenger RNA was determined in ventricular tissue. After 30 mins, TNF-alpha was undetectable in the coronary effluent However, 60 mins after the initiation of LPS infusion, TNF-alpha release was 875+/-255 pg/min and increased to 2164+/-721 pg/min at 150 mins. Simultaneous infusion of isoproterenol with LPS stimulated cyclic AMP release and inhibited TNF-alpha production. For instance, at 60 and 150 mins, TNF-alpha release was 75+/-38 and 58+/-29 pg/min, respectively (p < .05 vs. LPS alone). Simultaneous infusion of isoproterenol with LPS blocked the induction of TNF-alpha messenger RNA by LPS. Isoproterenol, begun 30 mins after the initiation of LPS infusion, still suppressed LPS-stimulated TNF-alpha release by 95% at 150 mins. Similar results were obtained with norepinephrine. Activation of beta-adrenergic receptors inhibits cardiac TNF-alpha release. This implies that cytokine production by the heart is inhibited by the sympathetic nervous system. In heart failure, the cardiac response to the sympathetic nervous system is impaired. This impairment may play a role in the high plasma levels of TNF-alpha found in heart failure.

Time course and prognostic significance of hemostatic changes in sepsis: relation to tumor necrosis factor-alpha.

To describe the time course and prognostic significance of tumor necrosis factor-alpha (TNF-alpha) levels and hemostatic abnormalities in clinical sepsis. Prospective, observational study with sequential measurements in an inception cohort. An emergency department in a university teaching hospital. Patients were followed up until they either left the hospital or died. During a 1-yr period, 43 adult patients were selected from all emergency department patients who met the established criteria for sepsis. Excluded were patients with either organ dysfunction or septic shock at the time of admission. None. Blood samples were collected serially (day of admission and on days 3, 5, and 7) to determine TNF-alpha, platelet count, fibrinogen, factor VII, antithrombin III, tissue-type plasminogen activator activity, plasminogen activator inhibitor activity, plasminogen, and alpha2-antiplasmin. Fibrinopeptide A was measured only on the day of admission. Data were analyzed to determine whether admission values or serially obtained values within 7 days were useful in predicting outcome. Thirteen patients died and 30 survived. On admission, assay values indicated that platelet count and antithrombin III were significantly lower than normal (as observed in 50 healthy adults). Fibrinogen, plasminogen activator inhibitor type 1, tissue-type plasminogen activator, fibrinopeptide A, and TNF-alpha were higher than normal, whereas concentrations of factor VII, plasminogen, and alpha2-antiplasmin were in the normal range. No differences were detected in the admission values between survivors and nonsurvivors, except for antithrombin III. However, subsequent values of some variables demonstrated a difference between survivors and nonsurvivors. Survivors showed increasing platelet count and antithrombin III values compared with nonsurvivors, in whom the values remained low, with no significant changes during the study period. High TNF-alpha levels were found in both groups, but only survivors experienced progressive decrease during the observation period. Early clinical sepsis is characterized by high plasma levels of TNF-alpha and by activation of the coagulation and fibrinolysis systems. Longitudinal analysis of some variables (antithrombin III, platelet count, and TNF-ea) showed some differences with time between the survivor and nonsurvivor groups, but we feel that such differences were not large enough to be predictive in individual patients.

Persistent Elevation of Inflammatory Cytokines Predicts a Poor Outcome in ARDS: Plasma IL-1β and IL-6 Levels Are Consistent and Efficient Predictors of Outcome Over Time

Inflammatory cytokines have been related to the development of adult respiratory distress syndrome (ARDS), shock, and multiple organ dysfunction syndrome (MODS). We tested the hypothesis that unfavorable outcome in patients with ARDS is related to the presence of a persistent inflammatory response. For this purpose, we evaluated the behavior of inflammatory cytokines during progression of ARDS and the relationship of plasma inflammatory cytokines with clinical variables and outcome.We prospectively studied 27 consecutive patients with severe medical ARDS. Plasma levels of tumor necrosis factor alpha (TNF-alpha) and interleukins (ILs) 1 beta, 2, 4, 6, and 8 were measured (enzyme-linked immunosorbent assay [ELISA] method) on days 1, 2, 3, 5, 7, 10, and 12 of ARDS and every third day thereafter while patients were receiving mechanical ventilation. Subgroups of patients were identified based on outcome, cause of ARDS, presence or absence of sepsis, shock, and MODS at the time ARDS developed. Subgroups were compared for levels of plasma inflammatory cytokines on day 1 of ARDS and over time.Of the 27 patients, 13 survived ICU admission and 14 died (a mortality rate of 52%). Overall mortality was higher in patients with sepsis (86 vs 38%, p < 0.02). The mean initial plasma levels of TNF-alpha, IL-1 beta, IL-6, and IL-8 were significantly higher in nonsurvivors (p < 0.0001) and in those patients with sepsis (p < 0.0001). Plasma levels of IL-1 beta (p < 0.01) and IL-6 (p = 0.03) were more strongly associated with patient outcome than cause of ARDS (p = 0.8), lung injury score (LIS), APACHE II score, sepsis (p = 0.16), shock, or MODS score. Plasma levels of TNF-alpha, IL-1 beta, IL-6, and IL-8 remained significantly elevated over time (p < 0.0001) in those who died. Although it was the best early predictor of death (p < 0.001), plasma IL-2 > 200 pg/mL lost its usefulness after the first 48 h. A plasma IL-1 beta or IL-6 level > 400 pg/mL on any day in the first week of ARDS was associated with a low likelihood of survival.Our findings indicate that unfavorable outcome in acute lung injury is related to the degree of inflammatory response at the onset and during the course of ARDS. Patients with higher plasma levels of TNF-alpha, IL-1 beta, IL-6, and IL-8 on day 1 of ARDS had persistent elevation of these inflammatory cytokines over time and died. Survivors had lesser elevations of plasma inflammatory cytokines on day 1 of ARDS and a rapid reduction over time. Plasma IL-1 beta and IL-6 levels were consistent and efficient predictors of outcome.