Biomedical subjects

M Ceska

Publications and source records attributed to M Ceska.

At least 19 recordsLinked to original sources

PubMed1997

Interleukin-8 expression in patients after renal transplantation.

Cellular invasion and cytokine release are important steps in the initiation of rejection. We studied the release of interleukin-8 (IL-8), a potent proinflammatory and chemotactic cytokine, and its prognostic significance in predicting rejection after renal transplantation. Serum and urine samples were analyzed with an IL-8-specific sandwich enzyme-linked immunosorbent assay. Biopsy tissue specimens (n = 20) were snap-frozen and examined with immunohistochemistry using two monoclonal antibodies against human IL-8 (4G9 and 2A8). Serum IL-8 measurements were of no value in predicting rejection due to low sensitivity (24%). In 45 biopsy-proven acute rejections (< 2 months after transplantation), urinary IL-8 concentrations were elevated in 62% (298 +/- 54 pg/mL; P < 0.01), preceding clinical diagnosis of rejection. After treatment, the IL-8 concentration in urine decreased back to normal (33 +/- 4 pg/mL; P < 0.01). The highest urinary IL-8 concentrations were seen in patients with biopsy-proven rejection in combination with acute tubular necrosis (610 +/- 150 pg/mL). This finding was independent of renal function and urinary volume. Only three of 15 rejection episodes in patients more than 2 months after transplantation showed an elevated IL-8 concentration in urine (94 +/- 60 pg/mL). In 10 of 23 patients with infection, a significant increase of IL-8 in urine was observed as well (157 +/- 67 pg/mL; P < 0.05). IL-8-positive staining was found within interstitial mononuclear cells of all biopsy specimens showing rejection. Additionally, the antibody 4G9 stained arteriolar smooth muscle and tubular cells. Interestingly, a few IL-8-positive cells were present in two donor kidneys before transplantation was performed; control tissue was negative. Further investigations are necessary to determine the clinical value of urinary IL-8 determinations in the diagnosis of rejection and to evaluate the role of IL-8 in the pathogenesis of acute allograft rejection.

Enzyme-Linked Immunosorbent Assay↗

PubMed1996

The effect of simian immunodeficiency virus infection in vitro and in vivo on the cytokine production of isolated microglia and peripheral macrophages from rhesus monkey.

Microglia are the major target for human immunodeficiency virus (HIV) infection within the central nervous system. Because only a few cells are productively infected, it has been suggested that an aberrant cytokine production by this cell population may be an indirect mechanism leading to the development of neurological disorders in HIV-infected patients. Therefore we decided to study the secretion pattern of several interleukins (IL) by microglial cells and peripheral blood macrophages isolated from uninfected and simian immunodeficiency virus (SIV)-infected Rhesus monkeys. We found that uninfected, unstimulated primate microglia produce more IL-6 and less TNF alpha than peripheral blood macrophages, but generate comparable levels of IL-1 beta and IL-8. After infection with SIV in vitro, synthesis of all cytokines tested is increased compared to uninfected cultures and to peripheral blood macrophages. Microglia isolated from infected animals produce more IL-8 and TNF alpha than the uninfected cultures and display a strongly increased capacity to secrete TNF alpha upon stimulation with lipopolysaccharide. In addition, production of IL-6 by in vivo-infected microglia increases with time in culture to very high levels despite the fact that only a few cells contained replicating virus. These findings clearly show that the cytokine production of microglia is impaired after SIV infection both in vitro and in vivo and that a low level of viral replication is sufficient for these alterations to occur. In conclusion, the results of this study further support a possible role of cytokines in the pathogenesis of neuro-AIDS.

Animals↗

PubMed1995

beta-Amyloid(25-35) induces the production of interleukin-8 from human monocytes.

In an effort to unravel some of the cellular actions of beta-amyloid protein (A beta), we investigated its effects on interleukin-8 (IL-8) production from human monocytes. Supernatants harvested from cultured monocytes stimulated with the neurotoxic fragment 25-35 of beta-amyloid [A beta(25-35)] contained significant amounts of IL-8. Northern blot analysis demonstrated that A beta(25-35) also induced IL-8 mRNA accumulation. The effect of A beta(25-35) on IL-8 mRNA accumulation and secretion was not mimicked by a scrambled A beta(25-35) peptide, and was not affected by polymyxin B sulphate, which, on the other hand, almost completely abolished the effect of lipopolysaccharide. Our results uncover a new biological action of beta-amyloid: that of stimulating the production of a chemokine from monocytes.

Amino Acid Sequence↗

PubMed1995

Effect of Pseudomonas aeruginosa on interleukin-8 release from human phagocytes.

Pseudomonas aeruginosa infections are commonly observed in sepsis, burns, as well as cystic fibrosis (CF). Among the professional phagocytes neutrophils and monocytes are recruited by various chemotactic factors from the cellular environment. Although they provide the first line of host defense excessive neutrophil accumulation seems to be a major cause of pathogenesis during P. aeruginosa infection. Interleukin-8 (IL-8) represents one important chemoattractant for professional phagocytes. To evaluate IL-8 releasability by phagocytes in the context of P. aeruginosa infection and especially of CF, we stimulated human polymorphonuclear neutrophilic granulocytes (PMN) and peripheral blood mononuclear cells (PBMC) as a source for monocytes with clinical P. aeruginosa isolates, with mucoid P. aeruginosa strain (CF3M) and its nonmucoid revertant (CF3), and with purified P. aeruginosa mucoid exopolysaccharide (alginate). A significant increase in IL-8 release as compared to unstimulated cells was observed after an incubation time of 90 min for PMN and after 60 min for PBMC which increased (PMN: up to 60-fold; PBMC: up to 40-fold) over time (up to 4 h). In contrast of PBMC, when PMN were studied, intracellular IL-8 exceeded the IL-8 release in unstimulated as well as in stimulated cells by up to 10-fold. All clinical P. aeruginosa isolates, independent of the clinical source, induced IL-8 release from human PBMC and PMN in a dose- and time-dependent manner.(ABSTRACT TRUNCATED AT 250 WORDS)

Alginates↗

PubMed1995

Plasma interleukin 8 and polymorphonuclear leukocyte elastase concentrations in patients with septic shock.

We determined the plasma concentrations of interleukin 8 (IL-8), polymorphonuclear leukocyte elastase (PMNE), and endotoxin in patients with septic shock in order to investigate the role of IL-8 and PMNE in the development of septic shock, especially in septic adult respiratory distress syndrome (ARDS). The IL-8 concentration in patients with septic shock was 6.28 +/- 9.00 ng/mL (mean +/- SD, n = 29), which was significantly higher (P < 0.0001) than the concentration in septic patients without shock (0.35 +/- 0.35 ng/mL, n = 40). There was a significant correlation between the IL-8 concentration and the PMNE concentration at the onset of septic shock (r = 0.6916, P < 0.0001). The IL-8 concentration was also significantly correlated with the endotoxin concentration (r = 0.5584, P = 0.0016). There was a significant negative correlation (r = -0.8237, P < 0.0001) between the serum PMNE concentration and the oxygenation index (PaO2/FiO2) at the onset of septic shock. These results indicate that IL-8 and PMNE are produced in large quantities when septic shock occurs, and may play a role in the development of septic ARDS.

Adult↗

PubMed1994

Serum levels of interleukin 6, interleukin 8, and C-reactive protein after human allogeneic bone marrow transplantation.

Serum levels of interleukin 6 (IL-6) and C-reactive protein (CRP) were measured every second day from day -6 to day +86 in 24 patients undergoing allogeneic (n = 23) and syngeneic (n = 1) bone marrow transplantation (BMT). Endogenous serum levels of IL-6, IL-8, and CRP were further analyzed during complications after BMT, such as fever of unknown origin (FUO), severe infectious complications and acute graft-versus-host disease (GVHD). In addition, CRP levels were measured in 10 patients with interstitial pneumonitis of various origins (CMV, idiopathic). In all 24 patients IL-6 and CRP levels showed a characteristic monophasic pattern. After a slight decrease in the first days after BMT, a significant increase was observed, starting on day +3/+5 (P < 0.05) and reaching peak levels on day +9/+11 (P < 0.01). CRP had a similar pattern, with an increase in serum levels on day +3/+5 and maximum levels one to three days after the IL-6 peak was reached. The magnitude of the peak was related to the development of complications in the further course of BMT and was high in patients with and low in patients without complications. Serum levels of both molecules returned to baseline after day 14 posttransplant. Increased IL-6 and CRP levels were observed in the further course of BMT during severe infections or FUO either on the day of clinical onset (IL-6) or three days later (CRP), but not during acute GVHD grade III/IV. CMV interstitial pneumonitis (CMV-IP) was accompanied by an increase in CRP levels, while no such elevations were observed in patients with idiopathic interstitial pneumonitis (IIP). Elevated IL-8 serum levels occurred during bacterial infections, but to a lesser amount also during GVHD and CMV-IP. In conclusion, a characteristic pattern of IL-6 and CRP was observed after allogeneic BMT and a further increase associated with infectious complications. Since no significant elevations were seen in patients with GVHD, we conclude that both molecules are not involved in the induction of GVHD and might be useful diagnostic tools for the prediction and diagnosis of infectious complications after BMT. In contrast, assessment of IL-8 serum values does not permit clinical complications to be specified.

Adolescent↗

PubMed1994

Production of interleukin-1 receptor antagonist, inflammatory chemotactic proteins, and prostaglandin E by rheumatoid and osteoarthritic synoviocytes--regulation by IFN-gamma and IL-4.

This study analyzes the effects of the T cell cytokines IL-4 and IFN-gamma on the spontaneous and stimulated production of IL-8, MCP-1, IL-1 receptor antagonist (IL-1ra), and PGE by synoviocytes from rheumatoid arthritis (RA) and osteoarthritis (OA) patients. Cells from both sources constitutively released IL-8 and MCP-1, but no IL-1ra or PGE. Stimulation with IL-1 beta or TNF-alpha massively increased chemokine production and induced the generation of PGE and low amounts of IL-1ra. The constitutive or cytokine-stimulated release of IL-8 was inhibited by IFN-gamma, but not by IL-4. The constitutive or IL-1 beta-stimulated release of MCP-1, by contrast, was markedly enhanced by IL-4 and IFN-gamma. Both cytokines, however, had only borderline effects on the release stimulated by TNF-alpha. The yield of IL-1ra was strongly enhanced by IFN-gamma in all cases, whereas the effect of IL-4 was pronounced only in IL-1 beta-stimulated OA synoviocytes. IL-4, on the other hand, markedly decreased the release of PGE, which was less susceptible to IFN-gamma. The observed effects on chemokines, IL-1ra expression, and PGE release by synoviocytes suggest that IFN-gamma and IL-4 are important regulatory elements in the inflamed synovium and may exert anti-inflammatory effects.

Arthritis, Rheumatoid↗

PubMed1994

Modulation of proinflammatory cytokine release from human polymorphonuclear leukocytes by gamma interferon.

Polymorphonuclear leukocytes (PMN) have been identified as important sources of various proinflammatory cytokines. Since Interferon-gamma (IFN-gamma) is one of the activating factors of PMN, we have examined its effect on PMN-derived cytokine production. Recently, we demonstrated that IFN-gamma inhibits the release of IL-8 by PMN stimulated for 2 with different agonists. In this report, we show that the IFN-gamma-dependent inhibition of IL-8 release by PMN stimulated with lipopolysaccharide (LPS), tumor necrosis factor (TNF), and/or interleukin-1 beta (IL-1 beta), but not with Y-IgG, is a transient phenomenon. Indeed, PMN stimulated in the presence of IFN-gamma for 18 hr demonstrated an enhanced expression of IL-8 antigen in cell-free supernatants compared with stimuli alone. This enhanced accumulation of IL-8 partially reflected changes at the level of cell-associated versus cell-secreted IL-8 as PMN incubated with IFN-gamma secreted significantly more IL-8, relative to untreated cells. Unlike IL-8, the LPS-stimulated production of TNF and IL-1 beta, as well as the TNF-stimulated production of IL-1 beta, was markedly enhanced by IFN-gamma over the entire incubation period (up to 18 hr). Addition of anti-TNF and anti-IL-1 beta antibodies to IFN-gamma plus LPS-treated PMN indicated that the LPS-induced production of endogenous TNF and IL-1 beta, which was further potentiated by IFN-gamma pretreatment, mediated in autocrine fashion the enhanced LPS-induced IL-8 accumulation observed at 18 hr. Furthermore, as shown by Northern blot analysis, all the effects of IFN-gamma on LPS-stimulated PMN were paralleled by changes at the level of TNF, IL-1 beta, and IL-8 mRNA expression. Taken together, these findings identify novel biological actions of IFN-gamma as a modulator of the acute inflammatory response.

Cytokines↗

PubMed1994

Plasma endotoxin and cytokine concentrations in patients with hemorrhagic shock.

OBJECTIVES: The roles of cytokines and endotoxin in hemorrhagic shock, particularly the translocation of endotoxin and bacteria during hemorrhagic shock, were investigated. DESIGN: Prospective study. SETTING: Critical care and emergency center of a university hospital. PATIENTS: Twenty-nine patients with hemorrhagic shock and 20 healthy controls. INTERVENTIONS: Serial blood samples were collected from both study and control patients. Standard resuscitation techniques were used. MEASUREMENTS AND MAIN RESULTS: Plasma levels of endotoxin and various cytokines were determined repeatedly during hemorrhagic shock. Endotoxin was measured using an endotoxin-specific assay in addition to a new perchloric acid method for pretreatment of plasma. Cytokines were measured by commercial enzyme-linked immunosorbent assays. Plasma endotoxin concentrations remained within the normal range for 7 days after admission. Although levels of tumor necrosis factor-alpha and several interleukins increased slightly in some patients, these cytokines did not reach the levels seen in septic shock. CONCLUSIONS: Translocation of bacteria or endotoxin from the gastrointestinal tract into the bloodstream has been noted in animal experiments; however, translocation was not detected in our patients with hemorrhagic shock.

Adolescent↗

PubMed1994

Uroepithelial cells are part of a mucosal cytokine network.

This study compared the cytokine production of uroepithelial cell lines in response to gram-negative bacteria and inflammatory cytokines. Human kidney (A498) and bladder (J82) epithelial cell lines were stimulated with either Escherichia coli Hu734, interleukin 1 alpha (IL-1 alpha), or tumor necrosis factor alpha (TNF-alpha). Supernatant samples were removed, and the RNA was extracted from cells at 0, 2, 6, and 24 h. The secreted cytokine levels were determined by bioassay or immunoassay; mRNA was examined by reverse transcription-PCR. The two cell lines secreted IL-6 and IL-8 constitutively. IL-6 and IL-8 mRNA were constitutively produced in both cell lines; IL-1 beta mRNA was detected in J82 cells. IL-1 alpha induced significantly higher levels of IL-6 secretion than did E. coli Hu734 or TNF-alpha. IL-1 alpha and TNF-alpha induced significantly higher levels of IL-8 secretion than did E. coli Hu734. Secreted IL-1 beta was not detected; IL-1 alpha and TNF-alpha were not detected above the levels used for stimulation. IL-1 alpha, IL-1 beta, IL-6, and IL-8 mRNAs were detected in both cell lines after exposure to the stimulants. TNF-alpha mRNA was occasionally detected in the J82 cell line after TNF-alpha stimulation. Cytokine (IL-6 and IL-8) and control (glyceraldehyde 3-phosphate dehydrogenase [G3PDH] and beta-actin) mRNA concentrations were quantitated with internal PCR standards. Cytokine mRNA levels relative to beta-actin mRNA levels were the highest in E. coli-stimulated cells. In comparison, the cytokine mRNA levels relative to G3PDH mRNA levels were the highest in IL-1 alpha-stimulated cells. beta-Actin mRNA levels decreased after bacterial stimulation but not after cytokine stimulation, while G3PDH mRNA levels increased in response to all of the stimulants tested. These results suggested that E. coli Hu734 lowered the beta-actin mRNA levels in uroepithelial cells, thus distorting the IL-6 and IL-8 mRNA levels relative to this control. In summary, E. coli IL-1 alpha and TNF-alpha were found to activate the de novo synthesis and secretion of IL-6 and IL-8 in uroepithelial cells. These results emphasize the role of epithelial cells in cytokine-mediated responses during the early stages of infection.

Actins↗

PubMed1994

Polarised interleukin 8 secretion by HT 29/19A cells.

Interleukin 8 is a neutrophil chemotactic and stimulating cytokine induced by various inflammatory stimuli, including tumour necrosis factor, interleukin 1, and endotoxin. The ability of HT 29/19A enterocytes to synthesise interleukin 8 was studied. The results show that interleukin 1 is an important stimulus for interleukin 8 synthesis and secretion by HT 29/19A cells, being more potent than tumour necrosis factor. The tumour necrosis factor and interleukin 1 induced interleukin 8 secretion by HT 29/19A cells was seen to be polarised according to the direction of stimulation. These results support the concept that mucosal cells (enterocytes) may play an important part in initiating mucosal inflammation. Furthermore, it is proposed that HT 29/19A cells constitute a tool to study stimulus directed polarised cytokine secretion.

Calcimycin↗

PubMed1994

Effect of hemodialysis on peripheral blood monocyte tumor necrosis factor-alpha, interleukin-6, and interleukin-8 secretion in vitro.

The influence of blood-membrane interaction on human peripheral blood monocyte tumor necrosis factor-alpha (TNF), interleukin-6 (IL-6), and interleukin-8 (IL-8) secretion was measured during hemodialysis of end-stage renal disease patients by in vitro stimulation of whole blood with lipopolysaccharide. Monocyte TNF and IL-6 secretion in vitro was reduced 30 min after start of dialysis session. In contrast, cellular IL-8 secretion did not change during hemodialysis. Comparison of the results of three different membranes indicates that the bioincompatibility of the dialysis membrane was reflected in both leukocytopenia and reduction of cellular TNF secretion. During treatment of normal whole blood in an ex vivo dialysis closed-loop circuit, the ability of monocytes to release TNF, IL-6, and IL-8 in vitro remained constant. This indicates that the reduced IL-6 and TNF secretion during standard hemodialysis was not due to a direct effect of contact between dialysis membranes and monocytes, but rather was a result of redistribution within the patients' leukocyte pool.

Adult↗

PubMed1994

Effect of substance P on superoxide anion and IL-8 production by human PMNL.

The neuropeptide substance P (SP), a main mediator of neurogenic inflammation, has been shown to have direct and modulatory effects on functional responses of polymorphonuclear leucocytes (PMNL). In this study, we further investigated the effects exerted by SP on human PMNL functions. Pretreatment of PMNL with SP resulted in an increase of superoxide anion (O2-) production in response to formyl-methionyl-leucyl-phenylalanine (FMLP), concanavalin A (Con A) and opsonized zymosan (STZ). In contrast, the O2- production induced by tumour necrosis factor (TNF) was strongly inhibited by pretreatment with SP. Both enhancement and inhibition of O2- response were exerted by SP in a dose-dependent manner and at concentrations which did not directly stimulate O2- production. These effects were rapid in onset, and occurred after 5 min of preincubation of cells with the neuropeptide. At concentrations that modulated O2- production by PMNL, SP also directly stimulated release of the chemotactic cytokine interleukin-8 (IL-8). Induction of IL-8 release required a longer incubation time (1 hr) with SP and was preceded by an increase of IL-8 mRNA steady-state levels. Furthermore, as well as directly stimulating IL-8 production, SP was also able to enhance the IL-8 release induced by other stimuli such as FMLP and TNF. The results of this study indicate that, in addition to the rapid and differential modulation of O2- production, SP also induces long-term changes such as IL-8 synthesis and release, and can thus amplify the process of PMNL recruitment to the inflammatory site.

Concanavalin A↗

PubMed1993

Interleukin 10 (IL-10) inhibits the release of proinflammatory cytokines from human polymorphonuclear leukocytes. Evidence for an autocrine role of tumor necrosis factor and IL-1 beta in mediating the production of IL-8 triggered by lipopolysaccharide.

In this study we have examined the effects of interleukin 10 (IL-10) on polymorphonuclear leukocytes (PMN), and found that it is a potent inhibitor of tumor necrosis factor (TNF), IL-1 beta, and IL-8 secretion triggered by lipopolysaccharide (LPS). Cytokine production by phagocytosing PMN was also inhibited by IL-10, but to a lesser extent than the LPS-induced production. As shown by Northern blot analysis, IL-10 diminished the levels of TNF, IL-1 beta, and IL-8 mRNAs late after the onset of stimulation of PMN with LPS. In addition, we provide evidence that the kinetics of LPS-induced IL-8 production by PMN is composed of two distinct phases. Specifically, our experiments demonstrated that in the first phase, the production of IL-8 is a process directly induced by LPS that lasts for some hours. After this early wave, a second phase begins that is sustained and leads to an elevated production of IL-8 that appears to be due to the endogenous release of TNF and IL-1 beta. This second wave can in fact be blocked by anti-TNF and anti-IL-1 beta neutralizing antibodies, and by IL-10 as the consequence of its downregulatory effects on TNF and IL-1 beta release. Taken together, these findings identify novel biological actions of IL-10 as a suppressor of the inflammatory response.

Cells, Cultured↗

PubMed1993

Elevated interleukin-8 serum concentrations in beta-thalassemia and graft-versus-host disease.

Neutrophil chemotactic and functional defects occur in beta-thalassemia and in patients after bone marrow transplantation (BMT). Interleukin-8 (IL-8) is a novel chemotactic and activating peptide for neutrophils and can be detected in the circulation. IL-8 serum concentrations were evaluated in 30 beta-thalassemic patients before and after BMT. Serial samples from 16 patients were also studied. Fourteen sera from healthy children, 43 patients with chronic viral hepatitis, 16 patients on chronic transfusion treatment for various hematologic disorders, and 28 healthy adults were studied as controls. IL-8 was evaluated by an enzyme-linked immunosorbent assay. Patients with beta-thalassemia had higher IL-8 concentrations than did normal controls, patients with liver disease, and patients on chronic transfusion. beta-Thalassemic patients with severe liver siderosis and fibrosis had the highest IL-8 concentrations. After BMT in patients with successful engraftment, IL-8 concentrations decreased significantly. In contrast, in patients with acute graft-versus-host disease (GVHD), IL-8 concentrations were not statistically different from the concentrations found before BMT and were higher than in patients with no complications and patients with graft rejection. IL-8 may play a part in the immune dysregulation that occurs in beta-thalassemia and may be involved in the immune mechanisms leading to GVHD.

Adolescent↗

PubMed1993

Involvement of CD14 in lipopolysaccharide-induced tumor necrosis factor-alpha, IL-6 and IL-8 release by human monocytes and alveolar macrophages.

CD14 has been reported to function as a receptor for bacterial LPS complexed with serum proteins, transducing an activation signal for TNF-alpha production. We found that the anti-CD14 mAb MEM-18 inhibited not only LPS-induced release of TNF-alpha, but also LPS-induced, TNF-alpha independent release of IL-6 and IL-8 by human monocytes and alveolar macrophages. Inhibitory effect of MEM-18 was detected both in the presence of human or bovine calf serum and under serum-free conditions. In contrast, MEM-18 did not block release of these cytokines induced by IL-1 beta, TNF-alpha, PMA, and zymosan. We conclude that CD14 is involved in LPS-induced release of TNF-alpha, IL-6, and IL-8 by monocytes and alveolar macrophages and that this receptor appears to be able to recognize LPS directly in the absence of serum.

Antibodies, Monoclonal↗

PubMed1993

Studies on the regulatory mechanisms of interleukin-8 gene expression in resting and IFN-gamma-treated neutrophils: evidence on the capability of staurosporine of inducing the production of interleukin-8 by human neutrophils.

To understand how expression of IL-8 mRNA is regulated, we studied the effects of Staurosporine, H7, phorbol-myristate-acetate and Dexamethasone in human neutrophils subsequently treated with IFN-gamma. Our results can be summarized as follows: a) IL-8 mRNA steady state levels were enhanced in a dose dependent fashion by both Staurosporine and phorbol-myristate-acetate, were not influenced by H7, but were decreased by Dexamethasone; b) the negative effect of IFN-gamma on IL-8 mRNA accumulation was prevented by Staurosporine and phorbol-myristate-acetate, was not influenced by H7, and was potentiated by Dexamethasone; c) IL-8 mRNA induction caused by Staurosporine was accompanied by a time and dose dependent release of IL-8 into the PMN supernatants.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗

PubMed1993

The effect of replacement of dietary fat by palm oil on in vitro cytokine release.

In the present study the effect of replacement of dietary fat by palm oil in the normal Western diet on the in vitro release of the inflammatory cytokines tumour necrosis factor (TNF), interleukin (IL)-6 and IL-8 was examined. A maximal replacement of 700 g/kg dietary fat was achieved for thirty-eight male volunteers who consumed either a palm-oil diet or a control diet in a double-blind, cross-over study with 6-week experimental periods, and 3-week run-in and wash-out periods. At the end of both experimental periods, whole blood was stimulated in vitro with 0.02 (sub-optimal), or 10 ng lipopolysaccharide (LPS)/ml (maximal), whereafter TNF, IL-6, and IL-8 concentrations in the culture supernatant fraction were measured using specific enzyme-linked immunosorbent assays (ELISA). Mean cytokine production with sub-optimal, or maximal LPS stimulation of peripheral whole blood was similar for both the palm oil, and the control group. The relative TNF response, however, was reduced by replacement of dietary fat with palm oil. Separate analysis of the data from the first and second experimental periods strongly suggested that the residual effect of the palm-oil diet on the relative TNF response was longer than 9 weeks. Cytokine homeostasis determines the course of the inflammatory response and the progression of atherosclerosis. The effect of palm-oil consumption on the proneness of the peripheral blood cells to produce TNF may, therefore, alter the prevalence of these common diseases.

Adult↗