Erosion of a male polypropylene sling.
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Adult↗
Biomedical subjects
J Hakim
Publications and source records attributed to J Hakim.
Quality control in the screening of erectile dysfunction--results of a survey.
OBJECTIVES: To evaluate the screening patterns of primary care physicians with regard to erectile dysfunction (ED). METHODS: A prospective study was performed using an institutional review board-approved Sexual Health Inventory for Men questionnaire of male patients presenting to a university-based urology clinic. The data were compiled and analyzed with descriptive statistics using Statistical Package for Social Sciences, version 10.0, software. RESULTS: Of 140 patients, 102 completed and returned the survey. Of these patients, 93% were white. Twenty-five percent were between the ages of 40 and 50 years, 20% were between the ages of 51 and 60 years, and 24% were between the ages of 60 and 70 years. The average number of risk factors for ED identified in the patient population was 2.1. Fifty-six percent of patients had a Sexual Health Inventory for Men score of 21 or less, indicative of an element of ED. Eighty-three percent had primary care physicians; 23% of patients with a primary care physician were screened for ED. Of those screened, 58% of patients initiated the discussion with their physician. CONCLUSIONS: Screening for ED, using the Sexual Health Inventory for Men instrument, should be performed on patients with any identifiable risk factor. Screening is appropriate because effective treatment of ED is available and because ED can be associated with occult cardiac disease.
Adult↗
Protein kinase C zeta phosphorylates a subset of selective sites of the NADPH oxidase component p47phox and participates in formyl peptide-mediated neutrophil respiratory burst.
Generation of superoxide anion by the multiprotein complex NADPH phagocyte oxidase is accompanied by extensive phosphorylation of its 47-kDa protein component, p47(phox), a major cytosolic component of this oxidase. Protein kinase C zeta (PKC zeta), an atypical PKC isoform expressed abundantly in human polymorphonuclear leukocytes (PMN), translocates to the PMN plasma membrane upon stimulation by the chemoattractant fMLP. We investigated the role of PKC zeta in p47(phox) phosphorylation and in superoxide anion production by human PMN. In vitro incubation of recombinant p47(phox) with recombinant PKC zeta induced a time- and concentration-dependent phosphorylation of p47(phox) with an apparent K(m) value of 2 microM. Phosphopeptide mapping analysis of p47(phox) showed that PKC zeta phosphorylated fewer selective sites in comparison to "conventional" PKCs. Serine 303/304 and serine 315 were identified as targets of PKC zeta by site-directed mutagenesis. Stimulation of PMN by fMLP induced a rapid and sustained plasma membrane translocation of PKC zeta that correlated to that of p47(phox). A cell-permeant-specific peptide antagonist of PKC zeta inhibited both fMLP-induced phosphorylation of p47(phox) and its membrane translocation. The antagonist also inhibited the fMLP-induced production of oxidant (IC(50) of 10 microM), but not that induced by PMA. The inhibition of PKC zeta expression in HL-60 neutrophil-like cells using antisense oligonucleotides (5 and 10 microM) inhibited fMLP-promoted oxidant production (27 and 50%, respectively), but not that induced by PMA. In conclusion, p47(phox) is a substrate for PKC zeta and participates in the signaling cascade between fMLP receptors and NADPH oxidase activation.
Amino Acid Sequence↗
The role of phagocytes in HIV-related oxidative stress.
BACKGROUND: in response to a variety of stimuli, phagocytes release large quantities of reactive oxygen species (ROS), which are essential for bacterial killing. However, excessive ROS production not appropriately compensated by antioxidant molecules can lead to oxidative stress, which may also play an important role in pathogenesis of HIV infection. In fact, ROS participate in chronic inflammation, HIV replication and the apoptosis of cells of the immune system. OBJECTIVE AND STUDY DESIGN: we used flow cytometry to study, in whole blood, the activation and redox status of polymorphonuclear neutrophils (PMN) and monocytes at different stages of the disease. RESULTS: we showed that neutrophils and monocytes from HIV-infected patients spontaneously produced increased amounts of H2O2. This increased H2O2 production was associated with alterations of adhesion molecules expression at the cell surface, which also reflected basal activation of phagocytes from the HIV-infected patients. In monocytes, basal H2O2 production correlated with viral load. This increased ROS production was associated with changes in the expression of the antiapoptotic/antioxidant compounds Bcl-2 and thioredoxin along the course of the disease. This modulation could result from a dual regulation by oxidative stress and could explain at least in part why monocyte numbers remain relatively stable throughout the disease. Monocytes expressed a normal maximal capacity to produce ROS in optimal conditions of stimulation. In contrast, after ex vivo priming with TNFalpha or IL-8, neutrophils showed a decreased H2O2 production in response to bacterial N-formyl peptides. This latter impairment correlated with the decrease in CD4+ lymphocyte numbers and with IL-8 and IL-6 plasma levels. CONCLUSIONS: the increased basal ROS production by phagocytes could participate to the oxidative injury which has been implicated in the pathophysiology of HIV infection. In addition, the decreased priming of H2O2 production by neutrophils could contribute to the increased susceptibility of HIV-infected patients to bacterial infections.
Actins↗
Vascular endothelial growth factor production by fibroblasts in response to factor VIIa binding to tissue factor involves thrombin and factor Xa.
Tissue factor (TF) assembled with activated factor VII (FVIIa) initiates the coagulation cascade. We recently showed that TF was essential for FVIIa-induced vascular endothelial growth factor (VEGF) production by human fibroblasts. We investigated whether this production resulted from TF activation by its binding to FVIIa or from the production of clotting factors activated downstream. Incubation of fibroblasts with a plasma-derived FVIIa concentrate induced the generation of activated factor X (FXa) and thrombin and the secretion of VEGF, which was inhibited by hirudin and FXa inhibitors. By contrast, the addition of recombinant FVIIa to fibroblasts did not induce VEGF secretion unless factor X was present. Moreover, thrombin and FXa induced VEGF secretion and VEGF mRNA accumulation, which were blocked by hirudin and FXa inhibitors, respectively. The effect of thrombin was mediated by its specific receptor, protease-activated receptor-1; in contrast, the effect of FXa did not appear to involve effector cell protease receptor-1, because it was not affected by an anti-effector cell protease receptor-1 antibody. An increase in intracellular calcium with the calcium ionophore A23187 or intracellular calcium chelation by BAPTA-AM had no effect on either basal or FXa-induced VEGF secretion, suggesting that the calcium signaling pathway was not sufficient to induce VEGF secretion. Finally, FVIIa, by itself, had no effect on mitogen-activated protein (MAP) kinase activation, contrary to thrombin and FXa, which activate the p44/p42 MAP kinase pathway, as shown by the blocking effect of PD 98059 and by Western blotting of activated MAP kinases. These findings indicate that FVIIa protease induction of VEGF expression is mediated by thrombin and FXa generated in response to FVIIa binding to TF-expressing fibroblasts; they also exclude a direct signaling involving MAP kinase activation via the intracellular domain of TF when expressed by these cells.
Antithrombins↗
The deadly double infarct syndrome treated by two-vessel primary angioplasty and stenting.
Percutaneous transluminal primary angioplasty (PTCA) has become an accepted therapy for treatment of acute myocardial infarction. Coronary stenting in the setting of acute myocardial infarction has been found to have several advantages, and has been successfully performed routinely at various centers. However, we are unaware of any report that describes successful angioplasty performed on two simultaneously occluded coronary arteries (the deadly double infarct syndrome). This is the first report of successful primary angioplasty with stenting performed on a patient with occlusion of two vessels simultaneously. We review the literature and suggest that this may prove to be a viable alternative in an emergency in two-vessel coronary artery bypass grafting.
Angioplasty, Balloon, Coronary↗
Neutrophil dysfunctions, IL-8, and soluble L-selectin plasma levels in rapidly progressive versus adult and localized juvenile periodontitis: variations according to disease severity and microbial flora.
We used flow cytometry to analyze the expression of adhesion molecules and the oxidative burst of whole-blood polymorphonuclear neutrophils (PMN) from 26 patients with periodontitis. Three different clinical entities were studied: adult periodontitis (AP), localized juvenile periodontitis (LJP), and rapidly progressive periodontitis (RPP). Unstimulated PMN from the patients showed reduced Lewis x, sialyl-Lewis x, and L-selectin expression relative to those from healthy control subjects. These alterations were present whatever the severity of periodontal disease. However, PMN from RPP patients showed increased basal H2O2 production and decreased L-selectin shedding. These latter impairments, which correlated with increased IL-8 plasma levels, could contribute to initial vascular damage. In addition, decreased IL-8 priming of H2O2 production by PMN from RPP patients could account for a lower bactericidal capacity of PMN, leading to the large number of bacteria in the subgingival region of RPP patients. Soluble L-selectin plasma levels were also decreased in the RPP group, indicating more severe or diffuse endothelial damage. These abnormalities were not found in the patients with less destructive forms of periodontitis (AP and LJP). Porphyromonas gingivalis, a bacterial pathogen known to increase IL-8 production by PMN, was found in the periodontal pockets of RPP patients only. These results show links among PMN abnormalities, the clinical form of periodontitis, and the gingival bacterial flora.
Adolescent↗
P40phox associates with the neutrophil Triton X-100-insoluble cytoskeletal fraction and PMA-activated membrane skeleton: a comparative study with P67phox and P47phox.
NADPH oxidase is an O2*- -generating enzyme found in phagocytes such as neutrophils. It is composed of a membrane-bound cytochrome b, the cytosolic proteins p67phox, p47phox, p40phox, and the G-protein p21rac. The system is dormant in resting cells but acquires catalytic activity on exposure to appropriate stimuli. Cytochrome b, p67phox, p47phox, and rac2 associate with the cytoskeleton and membrane skeleton of activated neutrophils. It is not known whether p40phox associates with the cytoskeleton. The purpose of this study was to analyze the subcellular distribution of p40phox. When resting neutrophils were lysed in Triton X-100 or octyl glucoside buffer and separated into detergent-soluble and detergent-insoluble fractions, p40phox and p67phox were mainly associated with the detergent-insoluble fraction (defined as the cytoskeleton), whereas p47phox was mainly found in the soluble fraction. Neutrophil activation by phorbol myristate acetate (PMA) induced p47phox translocation to the cytoskeleton but did not affect the distribution of p40phox or p67phox. Using immunofluorescence confocal microscopy, we found that p40phox colocalized with filamentous actin. In neutrophils from a p67phox-deficient patient with detectable p40phox, p40phox associated with the cytoskeleton only after activation by PMA. A complex containing the three proteins was isolated from the cytoskeleton of activated neutrophils. When activated membranes were treated with Triton X-100 buffer, p40phox, p47phox, and p67phox were found in the membrane skeleton enriched in NADPH-oxidase activity; some p40phox and p47phox was found in the soluble membrane fraction, but no p67phox was detected. These findings show that p40phox, like p67phox and p47phox, binds to the cytoskeleton and membrane skeleton. In addition, p40phox can dissociate from p67phox in activated membranes.
Actins↗
Defective priming of the phagocyte oxidative burst in a child with recurrent intracellular infections.
Human phagocytes (polymorphonuclear neutrophils and monocytes) play a critical role in host defense against invading microorganisms. Recent studies reported that circulating phagocytes undergo a final maturation process, in particular in terms of oxidative burst, during extravasation and migration to local sites of inflammation. This process is known as priming. We report here on a nine-year-old boy with successive disseminated infections due to intracellular microorganisms (Mycobacterium bovis, BCG, and Salmonella typhimurium). No T- or B-cell quantitative or qualitative defects were found. Polymorphonuclear neutrophil (PMN) migration and NADPH oxidase in PMNs and monocytes stimulated with various agents at optimal concentrations were normal, ruling out a leukocyte adhesion deficiency syndrome, a Chediak Higashi syndrome, and a chronic granulomatous disease. Nevertheless, the patient's PMNs and monocytes showed defective priming capacity, as measured by H(2)O(2) production after pretreatment with LPS (5 microg/mL for 30 min), TNFalpha (100 units/mL for 30 min), or IL-8 (50 ng/mL for 30 min) in response to bacterial N-formyl peptides (fMLP 10(-6) M for 5 min). In these conditions, H(2)O(2) production of PMNs and monocytes from the patient did not exceed that of the samples treated with fMLP or LPS alone, while the controls strongly produced H(2)O(2). Moreover, monocytes from the patient showed an impaired capacity to kill S. typhimurium in vitro. Such an impairment could be related at least in part to the priming deficiency of phagocyte oxidative burst. This case suggests, for the first time, that in vivo priming processes are critical in host defence against intracellular pathogens.
Adult↗
Redox and activation status of monocytes from human immunodeficiency virus-infected patients: relationship with viral load.
Monocytes are precursors of tissue macrophages, which are major targets of human immunodeficiency virus type 1 (HIV-1) infection. Although few blood monocytes are infected, their resulting activation could play a key role in the pathogenesis of HIV disease by modulating their transendothelial migration and inducing the production of reactive oxygen species (ROS). ROS participate in chronic inflammation, HIV replication, and the apoptosis of immune system cells seen in HIV-infected subjects. Published data on monocyte activation are controversial, possibly because most studies have involved monocytes isolated from their blood environment by various procedures that may alter cell responses. We therefore used flow cytometry to study, in whole blood, the activation and redox status of monocytes from HIV-infected patients at different stages of the disease. We studied the expression of adhesion molecules, actin polymerization, and cellular levels of H2O2, Bcl-2, and thioredoxin. Basal H2O2 production correlated with viral load and was further enhanced by bacterial N-formyl peptides and endotoxin. The enhanced H2O2 production by monocytes from asymptomatic untreated patients with CD4(+) cell counts above 500/microliter was associated with a decrease in the levels of Bcl-2 and thioredoxin. In contrast, in patients with AIDS, Bcl-2 levels returned to normal and thioredoxin levels were higher than in healthy controls. Restoration of these antioxidant and antiapoptotic molecules might explain, at least in part, why monocyte numbers remain relatively stable throughout the disease. Alterations of adhesion molecule expression and increased actin polymerization could play a role in transendothelial migration of these activated monocytes.
Adult↗
Polymorphisms of the tissue factor pathway inhibitor (TFPI) gene in patients with acute coronary syndromes and in healthy subjects : impact of the V264M substitution on plasma levels of TFPI.
-Mutations of the gene encoding tissue factor pathway inhibitor (TFPI), an inhibitor of TF-induced activation of the coagulation cascade, were screened for in 130 patients and 142 healthy controls to determine whether these variants contribute to acute coronary syndromes or modify plasma TFPI levels. The following 3 new polymorphisms were identified: 384T-->C in exon IV, which does not change the corresponding amino acid (tyrosine 57); -33C-->T in intron 7 (the T/T, C/T, and C/C genotypes were found in approximately 50%, 40%, and 10% of subjects in both groups); and 874G-->A in exon IX (GTG-->ATG), which predicts a valine to methionine change (V264M) in the carboxy-terminus tail of TFPI. The V264M polymorphism was found in 9.2% of the cases and 4.9% of the controls; the associated odds ratio (OR) for acute coronary syndromes was 2.0 (95% confidence interval [CI], 0.7 to 5.1). The OR increased to 3.6 (95% CI, 0.8 to 15.7) and 3.2 (95% CI, 0.9 to 11.8) in nonsmokers and patients without other risk factors, respectively. The possible link between the V264M polymorphism and coronary heart disease was checked in a large case-control study of myocardial infarction (Etude Cas-Témoins de l'Infarctus du Myocarde [the ECTIM Study]). The results showed no link between the V264M polymorphism and coronary syndromes. Interestingly, however, 5 patients heterozygous for the V264M polymorphism had significantly lower plasma TFPI levels than did 13 patients with the most common genotype. Although our present results do not support an association between TFPI polymorphisms and acute coronary syndromes, the possibility that 1 of them, especially the exon IX polymorphism, is associated with subtypes of myocardial infarction or to evolutive particularities that were not assessed in this study, cannot be excluded and is currently being evaluated.
Acute Disease↗
Images in cardiovascular medicine: ruptured aneurysm of the sinus of Valsava.
A 27 year old woman presented with a two year history of cardiac symptoms. Echocardiographic examination revealed a ruptured aneurysm of the sinus of Valsava. Of note the patient was known to be HIV positive.
Adult↗
Monocyte expression of adhesion molecules in HIV-infected patients: variations according to disease stage and possible pathogenic role.
We used flow cytometry to study the expression of adhesion molecules at the cell surface and actin polymerization of whole-blood monocytes in 35 HIV-infected patients at different stages of the disease. Monocytes were activated in vivo, as demonstrated by increased expression of the adhesion molecule CD11b/CD18, reduced L-selectin antigen expression, and increased actin polymerization. These abnormalities were present in asymptomatic patients with CD4+ cell counts greater than 500/microl and did not increase with disease progression or viral load. Sialyl-Lewis x and CD31 expression at the monocyte surface was normal in asymptomatic and symptomatic non-AIDS patients. In contrast expression of both molecules was strongly reduced in patients with AIDS. This change, despite normal maximal CD11b/CD18 expression and normal maximal actin polymerization, could contribute to the increased susceptibility to bacterial infections in AIDS. In contrast enhanced monocyte activation may promote their transendothelial migration in non-AIDS patients, possibly explaining the macrophage infiltration that can occur early in the disease.
Actins↗
Tissue factor-dependent vascular endothelial growth factor production by human fibroblasts in response to activated factor VII.
The transmembrane protein tissue factor (TF) is the cell surface receptor for coagulation factor VII (FVII) and activated factor VII (FVIIa). Recently, TF has been identified as a regulator of angiogenesis, tumor growth, and metastasis. This study was designed to link the binding of FVII(a) to its receptor, TF, with the subsequent triggering of angiogenesis through vascular endothelial growth factor (VEGF) production by human lung fibroblasts. We report that incubation of fibroblasts, which express constitutive surface TF, with FVII(a) induces VEGF synthesis. FVII(a)-induced VEGF secretion, assessed by a specific enzyme-linked immunosorbent assay, was time- and concentration-dependent. VEGF secretion was maximal after 24 hours of incubation of the cells with 100 nmol/L FVII(a) and represented a threefold induction of the basal VEGF level. Reverse transcriptase-polymerase chain reaction analysis of VEGF detected three mRNA species of 180, 312, and 384 bp corresponding, respectively, to VEGF121, VEGF165, and VEGF189. A 2.5- to 3.5-fold increase was observed for the 180- and 312-bp transcripts at 12 and 24 hours, respectively. FVII(a)-dependent VEGF production was inhibited by a pool of antibodies against TF, pointing to the involvement of this receptor. On specific active-site inhibition with dansyl-glutamyl-glycinyl-arginyl chloromethyl ketone, FVIIa lost 70% of its capacity to elicit VEGF production. Consistent with this, the native form (zymogen) of FVII only had a 1.8-fold stimulating effect. Protein tyrosine kinase and protein kinase C are involved in signal transduction leading to VEGF production, as shown by the inhibitory effects of genistein and GF 109203X. The results of this study indicate that TF is essential for VIIa-induced VEGF production by human fibroblasts and that its role is mainly linked to the proteolytic activity of the TF-VIIa complex.
Cells, Cultured↗
Blindness associated with midfacial fractures.
PURPOSE: This study assessed the frequency of blindness associated with midfacial fractures and correlated this with the fracture pattern. PATIENTS AND METHODS: A retrospective analysis of 49 patients admitted with midfacial fractures from January 1995 to March 1997 was performed to determine the presence of posttraumatic blindness. The medical and radiological records of the patients with blindness were reviewed for age and sex, cause of the injury, type of facial fracture, type of ocular trauma, and probable cause of the blindness. RESULTS: Ten of the 49 patients lost vision in one eye (20% of all midfacial fractures and 22% of midface fractures involving the orbit). The possibility of blindness associated with facial fractures was directly related to the severity of injury. Road traffic accidents were the most common cause. Blindness was attributable to traumatic optic nerve injury in seven cases and a ruptured globe in three cases. CONCLUSIONS: The high frequency of blindness associated with midfacial fractures in this series was attributable to the predominance of road traffic accidents as the major cause and absence of an obligatory seat belt law. Early diagnosis of the exact nature of the ophthalmic injury and treatment are important, and involvement of the ophthalmologist is mandatory.
Accidents, Traffic↗
Priming of phosphatidic acid production by staurosporine in f-Met-Leu-Phe-stimulated human neutrophils--correlation with respiratory burst.
Staurosporine, a microbial alkaloid known as a potent though non specific PKC inhibitor, enhances the production of superoxide anion (respiratory burst) of human polymorphonuclear leukocytes (PMN) stimulated by chemoattractants such as f-Met-Leu-Phe (fMLP). To gain insights into the mechanisms of this priming, we analysed staurosporine effects on formation of second messengers issued from phospholipase D (PLD), i.e., phosphatidic acid (PA) and its dephosphorylated form, diglycerides (DG). PA and DG were measured by two methods, in mass and after the labelling of PMN with a phosphatidylcholine precursor, [3H]-1-O-alkyl-2-lyso-3-phosphatidylcholine. Treatment of labelled PMN with low concentrations of staurosporine (12.5 and 50 nM) which prime respiratory burst had no significant effect on basal amounts of tritiated PA and DG, but potentiated fMLP-mediated formation of [3H]PA and phosphatidylethanol (PEt) pointing to a priming of PLD activity. PA mass in resting PMN increased (approximately 80 +/- 7%) in the presence of high drug concentrations only (250-500 nM), with no change in basal DAG mass. Low staurosporine concentrations (6.25-25 nM) markedly potentiated PA mass formation induced by fMLP and positive correlation (R = 0.95) was found between enhanced superoxide formation and generation of PA but not DG. Furthermore, cytochalasin B, which is known to prime PA production induced by fMLP, synergised the priming of respiratory burst by staurosporine, which further suggests a functional role of PA. In contrast to staurosporine, the more selective PKC inhibitor GF109203X neither stimulated PLD nor primed fMLP-induced PLD or respiratory burst. These data indicate that priming of fMLP-mediated PMN respiratory burst by staurosporine correlates with PA formation. This priming may be linked to alteration of early signalling events upstream of PLD rather than to feedback inhibition of PKC.
Diglycerides↗
Analysis of choline and phosphorylcholine content in human neutrophils stimulated by f-Met-Leu-Phe and phorbol myristate acetate: contribution of phospholipase D and C.
ABSTRACT. We analysed changes in choline (CHO) and phosphorylcholine (PCHO) content of stimulated human polymorphonuclear leukocytes (PMNs) by a chemiluminescence assay to further examine the relative contributions of phospholipase D (PLD) and PLC to phosphatidylcholine (PC) breakdown. PLD activation was also analysed by measuring tritiated phosphatidic acid (PA) and diglycerides (GDs) in PMNs labelled with tritiated alkyl-lyso PC. Stimulation of PMNs with formyl-methionyl-leucyl-phenylalanine fMLP; 0.1 microM induced a weak elevation of mass choline (+25% of basal level) that was strongly potentiated in PMNs primed with cytochalasin B (+350% relative to the control value of 657+/-53 pmol/10(7) cells). CHO production was rapid and transient, peaking within 1 min, and ran parallel to that of tritiated PA. Thereafter, the amount of tritiated PA declined strongly (40% of maximum by 3 min), whereas the elevated choline content induced by fMLP plateaued for at least 5 min. Phorbol myristate acetate (PMA) sustained the formation of CHO for as long as 20 min, which correlated with that of [3H]PA in a time- and concentration-dependent manner. PCHO content of resting PMN leukocytes (1560 +/- 56 pmol/10(7) cells) was not modified after stimulation of PMNs with fMLP or PMA for at least 10 min, which argues against breakdown of phosphatidylcholine by PLC. For longer treatment (10-20 min), fMLP stimulated a significant enhancement of PCHO level, which occurred concomitantly with a decrease in CHO level, suggesting that choline kinase rather than PLC may be activated. Unlike fMLP, PMA stimulated a fall in PCHO between 10 and 15 min after PMN stimulation, pointing to different regulatory mechanisms of PCHO level. These data indicate that DG formation from PC in PMNs is mediated by PLD but not by PLC and show that chemiluminescence measurement of choline is a reliable index of PLD activation.
Choline↗
Heterogeneity in Lewis-X and sialyl-Lewis-X antigen expression on monocytes in whole blood: relation to stimulus-induced oxidative burst.
By using flow cytometric analysis of cells in whole blood expressing high levels of CD14, we found a subpopulation of monocytes (8% of total) with higher scatter parameters, high capacity to produce reactive oxygen species (ROS), stronger expression of Lewis-X (CD15), sialyl-Lewis-X, CD11b and CD18 antigens, as well as an increased polymerized actin content. The size of this subpopulation increased after stimulation with lipopolysaccharide at the expense of the remaining monocytes, suggesting that its features were inducible. The membrane increase in Lewis-X and sialyl-Lewis-X expression observed during this conversion was largely due to the translocation of these carbohydrate structures from intracellular pools. Moreover, this subpopulation behaved as a primed monocyte subpopulation producing large amounts of H2O2 in response to N-formyl-methionyl-leucyl-phenylalanine. Increased H2O2 production was inhibited not only by anti-CD14 but also by anti-CD15 and anti-sialyl-Lewis-X monoclonal antibodies when added before lipopolysaccharide. These results show that lipopolysaccharide priming is regulated, at least in part, by Lewis-X and sialyl-Lewis-X structures expressed on the monocyte membrane. All together, this highly reactive and inducible subpopulation of monocytes, which share phenotypic and functional characteristics with neutrophils, might play an important role in host defenses and inflammatory responses.
CD18 Antigens↗