PubMed Health⌕ Search

Biomedical subjects

S Chollet-Martin

Publications and source records attributed to S Chollet-Martin.

At least 55 records · Page 3Linked to original sources
PubMed1994

Modulation of the expression of the granulocyte adhesion molecule, CR3, by percutaneous transluminal coronary angioplasty and contrast media.

RATIONALE AND OBJECTIVES: The effects of percutaneous transluminal coronary angioplasty (PTCA) and iodinated contrast media on the functional state of polymorphonuclear leukocytes (PMN) were determined; the expression of the PMN adhesion molecule, CR3, was assessed. METHODS: CR3 expression was measured by flow cytometry in whole blood samples in vivo, before and after PTCA (n = 17) or coronary angiography (n = 16); and in vitro, before and after incubation of PMNs with iodinated contrast media (n = 5). RESULTS: CR3 expression (mean +/- standard error of the mean, arbitrary units) decreased significantly after PTCA (221 +/- 25 to 168 +/- 21, P < .005) and coronary angiography (297 +/- 43 to 218 +/- 25, P < .05). In vitro, there was a dose-dependent decrease of CR3 expression and a significant and strong inverse correlation between CR3 expression and the contrast agent concentrations regardless of the type of contrast agent used. CONCLUSIONS: These data suggest that PTCA does not activate circulating PMNs, and that contrast media decrease CR3 expression. Whether this is related to the systemic adverse effects of contrast media remains to be clarified.

Angioplasty, Balloon, Coronary↗
PubMed1994

Cytokine response to burn injury: relationship with protein metabolism.

Plasma levels of interleukin 1 beta (IL-1 beta), tumor necrosis factor alpha (TNF alpha), interleukin 6 (IL-6), and markers of protein metabolism were determined in 12 burn patients throughout the healing period (day 2 to 21 post-injury) to determine the pattern of variations in plasma cytokine concentration. To establish the relationship between cytokine production and the nutritional status a wide range of severity standpoints (burn surface area ranging from 9% to 82%) was chosen. Interleukin 6 levels were increased in all patients throughout the study period; maximum concentrations (615 +/- 198 pg/mL) were reached on day 4 and correlated (p < 0.01) with the extent of burn injury. Tumor necrosis factor alpha levels were also elevated; they were significantly higher on day 7 in the patients who developed sepsis than in the other patients (67 +/- 21 pg/mL vs. 20 +/- 7 pg/mL; p < 0.05) but did not correlate with the extent of burn injury. Interleukin 1 beta was rarely detected. Cortisolemia on day 7 was inversely correlated with levels of TNF alpha but not with those of IL-6. Interleukin 6 levels correlated positively with protein turnover (phenylalaninemia) and catabolism (3-methylhistidine/creatinine ratio) and negatively with levels of fibronectin and transthyretin. Our data indicate that the systemic cytokine response to burn injury is mainly represented by IL-6. These data also support the hypothesis that IL-6 is a key mediator of the variations in protein metabolism following burn injury.

Adult↗
PubMed1994

Differential priming effects of proinflammatory cytokines on human neutrophil oxidative burst in response to bacterial N-formyl peptides.

Cytokines such as tumor necrosis factor alpha (TNF-alpha), granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin 8 (IL-8), IL-6, IL-1 alpha, and IL-1 beta produced during the immune and inflammatory responses to bacterial stimuli have been reported to interact with polymorphonuclear neutrophil (PMN) activities. However, contradictory findings on their direct and priming effects on the PMN oxidative burst, which is essential for bacterial killing, have been reported. We have used a flow cytometry method to study the effects of these cytokines on the oxidative burst of PMN in whole blood to avoid PMN activation related to isolation procedures. None of the cytokines tested directly activated the PMN oxidative burst, but they did have differential priming effects on the oxidative burst in response to bacterial N-formyl peptides. TNF, GM-CSF, and IL-8 strongly primed a subpopulation of PMN to produce H2O2 in response to N-formyl-methionyl-leucyl-phenylalanine (FMLP), while IL-1 alpha, IL-1 beta, and IL-6 failed to do so. Furthermore, the addition of TNF, GM-CSF, or IL-8 to whole blood increased the capacity of a subpopulation of PMN to bind N-formyl peptides, a phenomenon that could account, at least in part, for the strong H2O2 production in response to FMLP after priming by the cytokines. The size of the primed hyperresponsive subpopulation was greater after priming with TNF or GM-CSF than after priming with IL-8. However, GM-CSF, TNF, and IL-8 at suboptimal concentrations cooperated in the induction of a subpopulation hyperresponsive to FMLP. These results show that, of the various proinflammatory cytokines tested, TNF, GM-CSF, and IL-8 strongly prime the PMN oxidative burst in response to bacterial peptides in whole blood and suggest that these cytokines may play a critical role in bacterial killing in vivo.

Cytokines↗
PubMed1993

Priming of polymorphonuclear neutrophils by tumor necrosis factor alpha in whole blood: identification of two polymorphonuclear neutrophil subpopulations in response to formyl-peptides.

We have used a cytofluorometric method to study the effect of tumor necrosis factor alpha (TNF) priming on the oxidative burst, FMLP-receptor expression and actin polymerization of whole blood polymorphonuclear neutrophils (PMN). This technique permits the study of single cells and, thus, allowed us to examine the responsiveness of PMN to TNF in whole blood. We found that TNF in whole blood strongly primed a subpopulation of PMN to produce H2O2 in response to FMLP stimulation, whereas TNF and FMLP alone did not have a significant effect. Furthermore, adding TNF to whole blood increased the capacity of a subpopulation of PMN to bind N-formyl peptides at 4 degrees C, a phenomenon that could account, at least in part, for the strong H2O2 production in response to FMLP after TNF priming. Dual-color cytometric analysis showed that TNF primed actin polymerization on the same subpopulation in response to FMLP. Because the PMN subpopulation, which strongly bound N-formyl peptides at 4 degrees C, was no longer detectable after 1 minute of incubation at 37 degrees C, our data suggest that TNF treatment of PMN in whole blood primes a subpopulation that actively cycles FMLP receptors. These results suggest that PMN in the circulation may respond weakly to bacterial peptides and that TNF may play a critical role in the induction of the oxidative burst in vivo.

Actins↗
PubMed1993

High levels of interleukin-8 in the blood and alveolar spaces of patients with pneumonia and adult respiratory distress syndrome.

There is ample experimental evidence that polymorphonuclear neutrophils (PMN) play a critical role in the pathogenesis of the adult respiratory distress syndrome (ARDS). Since interleukin-8 (IL-8) is a strong chemotactic factor for PMN, we measured IL-8 levels in plasma and bronchoalveolar lavage (BAL) fluid of 18 patients, 12 with ARDS and 6 with severe pneumonia uncomplicated by ARDS, all of whom had an increased number of PMN in BAL fluid. Seven healthy subjects served as controls. We found elevated levels of IL-8 in the alveolar spaces of all patients tested. Elevated BAL IL-8 levels were related to a fatal outcome and the presence of shock and correlated with a general clinical severity index (simplified acute physiological score). BAL fluid levels of IL-8 were significantly higher in patients with ARDS than in patients with pneumonia. In plasma, IL-8 levels were increased similarly in all patients and did not correlate with survival or the presence of shock. The BAL fluid-to-plasma ratio of IL-8 was significantly greater than that of tumor necrosis factor alpha, indicating higher local production of IL-8. Moreover, the presence of a primed subpopulation of blood PMN with respect to H2O2 production indicates that IL-8 may contribute to the neutrophil-mediated process in the pathogenesis of ARDS and pneumonia.

Adult↗
PubMed1993

Evidence for priming and activation of neutrophils early after coronary angioplasty.

OBJECTIVES: Percutaneous transluminal coronary angioplasty (PTCA) induces deep arterial wall injury and transient ischaemia. The aim of this study was to demonstrate that PTCA could result in priming or activation of the neutrophils and the complement system. METHODS: Blood was drawn from the coronary sinus before and immediately after PTCA in 7 patients and before and immediately after coronary angiography in 7 patients (to ensure that the changes observed after PTCA were not solely related to the angiographic procedure). Neutrophil priming was assessed ex vivo by whole blood chemiluminescence stimulated in vitro by formyl-methionyl-leucyl-phenylalanine, phorbol myristate and opsonized zymosan. Neutrophil activation was assessed by measurement of plasma lactoferrin. RESULTS: Whole blood chemiluminescence increased after PTCA, regardless of the stimulus used, while it did not after arteriography. After PTCA, lactoferrin increased 2-fold (p < 0.02) whereas after arteriography a non-significant increase was observed. Neutrophil count and adherence properties were not modified by either PTCA or arteriography. Total haemolytic complement (CH50), C3, C4 and B factor decreased slightly (7 to 16%) after both PTCA and arteriography. CONCLUSIONS: Early after PTCA, the neutrophil oxidative response, assessed by stimulated whole blood chemiluminescence, increased, suggesting a "priming" effect of PTCA on neutrophils. In addition, plasma lactoferrin levels increased, indicating neutrophil activation. Finally, there was a mild global activation of the complement system, most likely related to the contrast agent, and which may play a role in the "priming" process. Neutrophil priming and activation may participate in several phenomena occurring after angioplasty such as enhanced vasoconstriction and post-ischaemic myocardial dysfunction. In addition, it may participate in triggering local inflammatory processes.

Angioplasty, Balloon, Coronary↗
PubMed1993

[State of activation of polynuclear neutrophils and cytokines in acute respiratory distress syndrome in adults].

To gain further insight into the pathogenesis of the adult respiratory distress syndrome (ARDS), the authors studied possible relationships among the activation status of circulating polymorphonuclear neutrophils (PMN), cytokine levels, and the severity of lung injury in 31 patients: 15 with ARDS, 9 with severe pneumonia uncomplicated by ARDS, and 7 mechanically ventilated patients with neither ARDS nor pneumonia. Nine healthy subjects served as controls. Using flow cytometry, the authors identified a subpopulation of PMN with an increased capacity to generate hydrogen peroxide after stimulation ex vivo in all three patient groups; significantly higher values were found in those with ARDS. The PMN stimulation index, a reflection of the degree of hyperresponsiveness, correlated with elevated levels of tumor necrosis factor alpha (TNF-alpha) in plasma, and both spontaneous and lipopolysaccharide (LPS)-induced TNF-alpha production by cultured monocytes. These biological expressions of PMN activation and cytokine generation both correlated with indices of the severity of lung injury, but not with the overall clinical severity. In contrast, IL-6 and IL-1 beta showed little or no relationship with either the degree of lung injury or PMN hyperresponsiveness. We conclude that TNF alpha-primed PMN may play a major role in the pathogenesis of ARDS-associated lung injury.

Adult↗
PubMed1992

Subpopulation of hyperresponsive polymorphonuclear neutrophils in patients with adult respiratory distress syndrome. Role of cytokine production.

To gain further insight into the pathogenesis of the adult respiratory distress syndrome (ARDS), we studied possible relationships among the activation status of circulating polymorphonuclear neutrophils (PMN), cytokine levels, and the severity of lung injury in 31 patients: 15 with ARDS, nine with severe pneumonia uncomplicated by ARDS, and seven mechanically ventilated with neither ARDS nor pneumonia. Nine healthy subjects served as controls. Using flow cytometry, we identified a subpopulation of PMN with an increased capacity to generate hydrogen peroxide after stimulation ex vivo in all three patient groups; significantly higher values were found in those with ARDS. The PMN stimulation index, a reflection of the degree of hyperresponsiveness, correlated with elevated levels of tumor necrosis factor-alpha (TNF alpha) in plasma, and both spontaneous and lipopolysaccharide-induced TNF alpha production by cultured monocytes. These biologic expressions of PMN activation and cytokine generation both correlated with indices of the severity of lung injury, but not with the overall clinical severity. In contrast, IL-6 and IL-1 beta showed little or no relationship with either the degree of lung injury or PMN hyperresponsiveness. We conclude that TNF-alpha-primed PMN may play a major role in the pathogenesis of ARDS-associated lung injury.

Flow Cytometry↗
PubMed1991

Induction of tumour necrosis factor-alpha during haemodialysis. Influence of the membrane type.

Some of the secondary clinical effects induced by long-term haemodialysis in patients with end-stage renal failure have been related to an increased production of interleukin-1 (IL-1). We investigated the role of another cytokine which shares a number of biological properties with IL-1, tumour necrosis factor-alpha (TNF-alpha). In long-term haemodialysed patients, we found at the beginning of the dialysis increased plasma TNF-alpha levels and enhanced monocyte capacity to produce TNF-alpha spontaneously ex vivo. Non-haemodialysed uraemic patients also presented increased plasma TNF-alpha levels. During dialysis with cellulose acetate (CA) or polysulphone (PS) membranes, plasma TNF-alpha levels and the spontaneous and lipopolysaccharide-induced production of TNF-alpha by monocytes remained at predialysis levels. In contrast, when cuprophane membranes were used, there was a significant increase in plasma TNF-alpha levels and in both spontaneous (10-fold) and lipopolysaccharide-induced (seven-fold) ex vivo TNF-alpha production by monocytes. These results suggest that monocytes are stimulated during haemodialysis with the poorly biocompatible cuprophane membrane.

Adult↗
PubMed1990

Increased monocyte procoagulant activity independent of the lupus anticoagulant in patients with systemic lupus erythematosus.

Monocytes can play a role in the activation of coagulation via increased procoagulant activity (PCA). We investigated the level of monocyte PCA in 19 patients with systemic lupus erythematosus (SLE), given the high rate of thrombotic events in this condition. Nine of these subjects also presented the lupus anticoagulant (LA). The PCA generated by patient monocytes was significantly higher than control values and was identified as tissue factor-like. Moreover, the number of monocytes with membrane-associated D dimer, a parameter which we have shown to be correlated with the PCA expressed in vitro by endotoxin-activated monocytes, was also significantly increased. Serum from both groups of patients (i.e. SLE and SLE + LA) stimulated the generation of PCA by control monocytes. By contrast, purified IgG from both patient groups had the same effect as control IgG on PCA generation by control monocytes. The nature of the stimulating agent in the serum was not identified. In conclusion, increased monocyte PCA may account for the increased incidence of thrombosis in SLE patients, although other, superimposed, factors would appear to exist in SLE + LA patients, given the higher incidence of thrombosis in this subgroup.

Adult↗
PubMed1990

Production by K 562 cells of an inhibitor of adherence-related functions of human neutrophils.

Certain tumor cells generate factors that inhibit neutrophil chemotaxis. Our study was designed to explore whether such factors are produced by K 562 malignant cells and whether these have a broader effect in altering neutrophil functions. After 48 h of in vitro culture of K 562 cells, the culture medium and the cells were separated, lyophilized, and extracted with ethanol. These K 562 products, i.e., either the cell or supernatant extract, inhibited both nonstimulated locomotion and locomotion induced either by FMLP or activated serum. Furthermore, K 562 products inhibited neutrophil adherence and oxidative burst induced by opsonized zymosan, whereas oxidative burst induced by PMA or FMLP was not altered. K 562 products had an inhibitory effect on the PMN binding to iC3b-coated particles. They did not modify Mo1 expression of resting cells, did not alter the up-regulation of the receptor induced by FMLP but inhibited the FMLP-induced capping of Mo1 Ag. Con A capping was also inhibited. Actin polymerization in FMLP-stimulated PMN, as measured by flow cytometry and phalloidin binding to F-actin, was inhibited by K 562 products. The inhibitory factor present in K 562 products (cell and culture supernatant) was purified in three steps including gel filtration, ion-exchange chromatography, and IEF. The eluted active fraction corresponded to single band of about 8 kDa on SDS-PAGE. From these experiments, it is concluded that K 562 malignant cells in culture contain and release a low molecular mass factor (congruent to 8 kDa) that inhibits all adherence-related functions of neutrophils, whereas it does not alter FMLP- or PMA-induced oxidative burst. Further studies are needed to assess whether products of other tumor cells also act on the neutrophil by inhibiting adherence-related functions, Mo1 function and capping, and actin polymerization.

Actins↗
PubMed1990

Increased monocyte procoagulant activity in patients with systemic lupus erythematosus.

Monocytes can play a role in the activation of coagulation via increased procoagulant activity (PCA). We investigated the level of monocyte PCA in 19 patients with systemic lupus erythematosus (SLE), given the high rate of thrombotic events in this condition. 9 of these subjects also presented the lupus anticoagulant (LA). The PCA generated by patient monocytes was significantly higher than control values and was identified as tissue factor-like. Serum from both groups of patients (i.e. SLE and SLE + LA) stimulated the generation of PCA by control monocytes. By contrast, purified IgG from both patient groups had the same effect as control IgG on PCA generation by control monocytes. The nature of the stimulating agent in the serum was not identified. In conclusion, increased monocyte PCA may account for the increased incidence of thrombosis in SLE patients, although other, superimposed, factors would appear to exist in SLE + LA patients, given the higher incidence of thrombosis in this subgroup.

Adult↗
PubMed1989

Monocyte procoagulant activity and membrane-associated D dimer after knee replacement surgery.

We have recently shown that monocyte membrane-associated cross-linked fibrin derivatives (D dimer) can be evidenced by immunogold staining. Using this method, the procoagulant activity (PCA) expressed in vitro by endotoxin-stimulated monocytes has been found to correlate significantly with the number of D dimer-positive monocytes. The incidence of postoperative thrombosis in patients undergoing total knee replacement has been reported by Stulberg et al to be 57%. Since monocytes can play a role, via increased PCA, in the activation of intravascular coagulation, we sought to determine the level of monocyte PCA ex vivo after knee replacement surgery and its possible correlation with the number of D dimer-positive monocytes. Finally, we examined the possible link between these modifications and the occurrence of postoperative deep vein thrombosis (DVT). The PCA expressed by monocytes with or without suboptimal stimulation, the number of D dimer-positive monocytes and the plasma level of D dimer were measured pre- and post-operatively in 11 patients undergoing total knee replacement. Phlebography was performed on day 10 after surgery. A significant increase in the PCA of stimulated monocytes was observed on day 10 after surgery. Moreover, both the number of D dimer-positive monocytes and the plasma level of D dimer increased significantly post-operatively. The number of D dimer-positive monocytes correlated with both monocyte PCA and the plasma D dimer level. The relation between these parameters is discussed. However, neither monocyte PCA nor the number of D dimer-positive monocytes was found to correlate with the occurrence of deep vein thrombosis.

Adult↗
PubMed1988

Binding of an anti D dimer monoclonal antibody to endotoxin-activated monocytes. Demonstration by immunogold-silver staining.

Blood monocytes exposed to a variety of stimuli, of which endotoxin is a potent one, produce and express on their membrane a procoagulant activity (PCA) which can trigger the formation of pericellular fibrin. We have developed an immunogold silver method using a monoclonal anti-D dimer antibody to detect the presence of crosslinked fibrin in derivatives on the monocyte membrane. The in vitro PCA of endotoxin-stimulated monocyte was shown to correlate significantly with the number of D dimer-positive monocytes. We suggest that this method could be used to identify activated monocytes expressing increased PCA.

Antibodies, Monoclonal↗
PubMed1988

Increased CD1-positive cells in peripheral blood of AIDS and ARC patients.

CD1 monoclonal antibodies were assayed on peripheral blood mononuclear leukocytes (PBML) of type 1 human immunodeficiency virus (HIV1)-infected patients using immunogold technique. Using IOT6 monoclonal antibody, a significant increase of the CD1 positive cells per microliter of blood was found in acquired immunodeficiency syndrome (AIDS) and AIDS-related complex (ARC) patients (265 +/- 34/microliters, n = 44 and 491 +/- 64/microliters, n = 36, respectively) as compared to controls (108 +/- 11/microliters, n = 43, P less than 0.001). These findings were confirmed with four other CD1 monoclonal antibodies in six patients. Characterisation of these CD1 positive cells showed that they were double stained with either CD4 or CD8 monoclonal antibodies. Moreover, cytochemical analysis of these cells showed the absence of myeloperoxidase activity and ultrastructural examination did not reveal Birbeck granules, well known to characterise the Langerhans cells. Further investigations are warranted to assess the biological and clinical relevance of these findings.

AIDS-Related Complex↗