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PubMed1990

Nonsteroidal antiinflammatory agents inhibit upregulation of CD11b, CD11c, and CD35 in neutrophils stimulated by formyl-methionine-leucine-phenylalanine.

Nonsteroidal antiinflammatory drugs (NSAIDs) inhibit PMN aggregation, chemotaxis, degranulation, and superoxide anion production stimulated by synthetic formyl peptides. Many of these functions are dependent upon receptors for the complement components C3b and iC3b (CD35 and CD11b, respectively), or the adherence molecules CD11b and CD11c. Using flow cytometry and specific monoclonal antibodies, we studied the effects of the NSAID piroxicam and indomethacin on the upregulation of these cell surface proteins on PMNs stimulated with FMLP, C5a, or ionomycin. Incubation of PMNs at 37 degrees C increased the expression of all three of these surface proteins. A further increase was induced by stimulation with FMLP, C5a, or ionomycin. Both piroxicam and indomethacin inhibited FMLP-induced upregulation of CD11b, CD11c, and CD35, but neither drug affected the upregulation of these surface molecules induced by C5a or ionomycin. Furthermore, piroxicam had no effect on 37 degrees C-induced upregulation of any of the surface proteins, while indomethacin showed no effect on 37 degrees C-induced CD11b upregulation but suppressed CD11c and CD35 upregulation. Inhibition of surface protein upregulation by FMLP was not due to inhibition of FMLP binding to PMNs. We conclude that piroxicam and indomethacin inhibit FMLP receptor-mediated upregulation of CD11b, CD11c, and CD35 in PMNs, but have no effect on the upregulation of these molecules by ionomycin or C5a. These data suggest that piroxicam and indomethacin interfere with postreceptor signaling events specific to PMN stimulation by FMLP.

Adult↗
PubMed1996

Gender differences in neutrophil function and cytokine-induced neutrophil chemoattractant generation in endotoxic rats.

Several lines of evidence indicate sexual dimorphism in the immune response. We explored gender differences in phagocytosis by neutrophils (PMNs), CD11b/c expression, generation of cytokine-induced neutrophil chemoattractant (CINC) and the influence of developmental stages on some of these parameters. Phagocytosis by PMNs of reproductive female rats was not suppressed by anesthesia and surgery as it was in age-matched males. The phagocytic response to an endotoxir (ET) challenge was also higher in PMNs of reproductive females than in males or in prereproductive or postreproductive females. CINC generation in reproductive females was lower than in age-matched males. Phagocytosis in saline-treated postreproductive females was reduced compared to reproductive and prereproductive females, but was not different from adult males. CD11b/c expression was greater in PMNs of saline treated postreproductive females, than in reproductive or prereproductive animals, but an ET challenge upregulated CD11b/c expression to the same level in all three groups. No gender difference was observed in this parameter. These data indicate that in terms of phagocytosis PMNs of reproductive female rats are more resistant to the effects of anesthesia and surgery and respond to an ET challenge more vigorously than cells of age-matched males. CINC generation in adult rats is also gender dependent. The developmental stages in females modulate phagocytosis and beta 2-integrin expression in PMNs.

Age Factors↗
PubMed1994

Plasma concentrations of total/free and functional protein S are not decreased in systemic lupus erythematosus patients with lupus anticoagulant and/or antiphospholipid antibodies.

We conducted an investigation to clarify whether or not the levels of total, free, and functional protein S and C4-binding protein (C4bp) in plasma are decreased in systemic lupus erythematosus (SLE) patients, especially those with antiphospholipid antibody (aPL), which is known to be a causative factor of such complications as habitual abortion and arteriovenous thrombosis. Fifty patients with SLE were recruited as subjects of the study. Serum aPL (anticardiolipin, antiphosphatidyl serine, antiphosphatidyl inositol, and antiphosphatidic acid antibodies) were measured by ELISA. Lupus anticoagulant was determined by a PTT, KCT, and diluted RVVT. Furthermore, plasma concentrations of total, free, and functional protein S and C4bp were measured. There were no significant differences in the mean levels of total, free, or functional protein S and C4bp between aPL-positive, aPL-negative SLE patients, and the healthy controls. From these results, we concluded that the protein S level is not the sole factor causing complications, and that other factor(s) may be involved in the induction of such complications in this clinical setting.

Antibodies, Antiphospholipid↗
PubMed1992

Cerebral sinus thrombosis in a patient with hereditary protein S deficiency: case report and review of the literature.

Hereditary protein S deficiency is an established risk factor for venous thrombosis. The common sites of thrombosis are the deep leg and pelvic veins. We report on a 38-year-old female patient with hereditary protein S deficiency and a previous history of deep leg vein thrombosis, who developed thrombosis of the cerebral straight and superior sagittal sinus while taking oral contraceptives. The diagnosis was established by computerized tomography and carotid angiography. Lysis of the thrombus occurred during heparin treatment. The hereditary nature of protein S deficiency was documented by family studies, since nine additional family members deficient in protein S were identified. Nineteen published cases of cerebral vein thrombosis and a deficiency of either anti-thrombin III, protein C, or protein S were reviewed. Compared with patients without a deficiency state, the clinical features of cerebral vein thrombosis were similar except for an earlier onset and a positive medical history of venous thromboembolic events in a considerable number of patients.

Adult↗
PubMed2001

Increased histidine decarboxylase expression during in vitro monocyte maturation; a possible role of endogenously synthesised histamine in monocyte/macrophage differentiation.

OBJECTIVE: In this study the expression of histidine decarboxylase (HDC), the pivotal enzyme in histamine formation and the effect of endogenously produced histamine on differentiation antigens was examined during in vitro differentiation of human monocytes. MATERIAL AND TREATMENT: Human elutriated monocytes from healthy volunteers were incubated with macrophage colony stimulating factor (M-CSF) and the expression of HDC was followed at both mRNA and protein levels. To study the possible function of histamine we followed the expression of some cell surface markers (CD14, CD16, CD91, CD49d and CD11c) relevant for phagocytic differentiation upon incubation in the presence of different histamine inhibitors, an HDC inhibitor: S(+)-alpha-fluoromethyl-histidine HCl, (alphaFMH), a compound that disturbs the interaction of histamine with intracellular cyp450 moieties: N,N-diethyl-2-[4-(phenylmethyl) phenoxy]-ethanamine HCI, (DPPE); and H1 and H2 receptor antagonists, Triprolidine and Cimetidine. RESULTS: During in vitro culture of elutriated human monocytes, in the presence of M-CSF, the gene expression and biosynthesis of HDC was considerably increased. The various antihistamine agents decreased the expression of the cell surface markers examined in this study. CONCLUSIONS: These data support the elevation of HDC expression during human monocytic differentiation and the possibility that monocyte-derived histamine is partially involved in regulation of M-CSF induced in vitro human monocyte/macrophage phagocytic differentiation.

Antigens, CD↗
PubMed1997

Effect of linoleic acid, linoleic acid anilide, and arachidonic acid on the expression of adhesion molecules on human neutrophils.

The effects of linoleic acid, linoleic acid anilide, and arachidonic acid on the expression of CD11b/ CD18, CD11c/CD18 integrins and L-selectin on human neutrophils were studied by flow cytometry in a whole blood assay. None of these compounds had any effect on the basal expression of CD11b, CD11c, or L-selectin in the concentration range of 20-100 microM. However, linoleic acid at a concentration of 1000 microM slightly up-regulated CD11b and CD11c by a factor of 2.1 and 1.7, respectively. Linoleic acid, linoleic acid anilide, and arachidonic acid did not affect the formyl-methionyl-leucyl-phenylalanine induced up-regulation of CD11b or CD11c. However, linoleic acid and linoleic acid anilide slightly inhibited the phorbol myristate acetate (PMA)-induced expression of CD11b, which was decreased by 27 and 21% at concentrations of 100 and 1000 microM, respectively. Likewise, arachidonic acid at 40 microM inhibited the PMA-induced expression of CD11b by 19%. Our results suggest that linoleic acid, linoleic acid anilide, and arachidonic acid do not dramatically affect the expression of leukocyte adhesion molecules in a whole blood assay.

Anilides↗
PubMed1992

Expression of Fc-gamma-RIII and fibronectin in peripheral polymorphonuclear neutrophils with increased response to Fc stimulation in patients with juvenile periodontitis.

The nature of increased luminol-enhanced chemiluminescence (CL) in peripheral polymorphonuclear neutrophils (PMN) in juvenile periodontitis is of pathophysiological interest and may serve as a model for tissue damage caused by granulocytes. Activation of PMNs by opsonized Staphylococcus aureus was compared with that of Actinobacillus actinomycetemcomitans and Bacteroides gingivalis, regarded as being more specific for juvenile periodontitis. The CL was higher in the PMNs from the patients, independently of bacteria and mode of opsonization (autologous serum or gamma-globulin). Fc-gamma-RIII assessed on the washed fragments from peripheral PMNs was significantly (p < or = 0.005) lower in the patients with juvenile periodontitis than in their pair-matched healthy controls, while the content of fibronectin was higher (p < or = 0.032). However, when Fc-gamma-RIII and fibronectin were studied in fresh PMNs by flow cytometry no difference could be found between the two groups. The increased generation of CL of peripheral PMNs found in patients with juvenile periodontitis seems to be independent of humoral factors and of bacterial species and may be related to the properties of the PMN cell membranes.

Adult↗
PubMed1984

High resolution isoelectric focusing of immunoprecipitated proteins under denaturing conditions. A simple analytical method applied to the study of complement component polymorphisms.

A simple analytical method for the study of structural protein polymorphisms is described. It consists of the immunoprecipitation of non-radiolabeled proteins using monospecific polyclonal antibodies followed by isoelectric focusing (IEF) under completely denaturing conditions in vertical polyacrylamide slab gels. The method uses small amounts of sample (usually unfractionated plasma or serum), requires no sophisticated equipment and allows the screening of large numbers of samples with comparatively small effort. This method has been applied in the identification of 2 human complement-component polymorphisms, C4-binding protein (C4-bp) and factor H (beta 1H).

Antigen-Antibody Reactions↗
PubMed1993

Separation of different forms of the fourth component of human complement by fast protein liquid chromatography.

Disruption of the thiolester in native C4 yields a 'C4b-like C4' molecule (iC4) that functionally resembles C4b and is therefore probably accompanied by conformational changes in the C4 molecule. In most purified C4 preparations, iC4 and C4b are present to a variable extent. In this study we evaluated the use of fast protein liquid chromatography (FPLC) to resolve and isolate these various forms of C4. C4 was purified from fresh human plasma in a 4-step procedure that included barium citrate adsorption, polyethylene glycol 6000 (PEG) precipitation, Q-Sepharose Fast Flow and mono Q ion exchange chromatography. The final preparation appeared to be homogeneous on SDS-PAGE and under reducing conditions consisted of three bands that corresponded to the intact alpha, beta and gamma chains of C4. In some preparations the alpha' chain of C4b was also observed. On a Mono Q column the purified C4 preparations could be separated into three peaks that by hemolytic assay and SDS-PAGE were characterized as representing native C4, and monomeric and dimeric iC4 (or monomeric and dimeric C4b). Finally, the apparent KA of the various forms of C4 for C4b-binding protein (C4BP) was investigated. The monomeric iC4 and C4b species demonstrated similar C4BP binding affinity with an apparent KA of 5.6-6.4 x 10(8) M-1, whereas their dimeric forms demonstrated a higher affinity for C4BP with an apparent KA: 0.9-2.3 x 10(9) M-1. Binding of native C4 to C4BP was undetectable.

Animals↗
PubMed1988

Characterization of immune complexes detected by the 125I-C1q binding assay in breast cancer.

The aim of the present study was to isolate and characterize immune complexes measured by the 125I-C1q binding assay in breast cancer sera. The C1q binding assay detects immune complexes by their binding to 125I-C1q and subsequent precipitation with PEG. We purified the C1q binding material from these precipitates by superose 6 gel filtration and cation exchange chromatography. The isolation steps were monitored by the C1q binding assay and the purified material was analyzed by SDS--PAGE and immunodiffusion. The C1q binding material isolated from two breast cancer sera contained complexes of IgM, C4b binding protein (C4-bp), and C1q. The C4-bp fraction showed significant C1q binding activity which increased after the addition of IgM. This C4-bp was not different from C4-bp isolated from normal serum. The IgM fraction, however, differed from normal IgM by its binding to C4-bp and C1q and its stronger affinity to the cation exchange column. These unique properties were not due to rheumatoid factor activity. They might be caused by a different glycosylation pattern or by complex formation with an as yet unknown polysaccharide antigen.

Antibodies, Neoplasm↗
PubMed1990

Immunology of atherosclerosis: cellular composition and major histocompatibility complex class II antigen expression in aortic intima, fatty streaks, and atherosclerotic plaques in young and aged human specimens.

There is evidence that fatty streaks in arteries can transform into atherosclerotic plaques. Mononuclear cells, including both monocytes and lymphocytes, are among the first cells participating in the development of atherosclerosis of experimental animals. To investigate the roles of different cell types in human atherosclerosis, we enumerated and compared the cellular compositions of normal intima, the transition zone (the area between the normal intima and the core of fatty streaks), fatty streaks, and plaques in young (age 16-30 years) and aged (over 60 years) human specimens using double-staining immunofluorescence with a series of monoclonal and polyclonal antibodies. T lymphocytes, both T helper/inducer (70% of T cells) and T suppressor/cytotoxic (30%) phenotypes, were found in every stage of atherosclerosis, constituting 30 to 40% of total cells in fatty streaks and transition zones of young subjects, and occasionally even in normal intima. Seventy percent of these T cells were HLA-DR positive, which indicated that most of them were activated. Macrophages were most frequent in fatty streaks and around the necrotic core of plaques. Smooth muscle cells, increasing from 5 to 30% with lesion progression, were HLA-DR positive where activated T helper cells occurred in the vicinity. The intracellular presence of the invariant gamma chain confirmed that HLA-DR was actually synthesized by these smooth muscle cells. Endothelial cells were HLA-DR positive above those regions of the lesions where HLA-DR-positive cells had accumulated, but not in normal intima, again suggesting induction of HLA-DR expression by T-cell-derived gamma-interferon. Furthermore, most HLA-DR-positive cells were also identified as HLA-DP and HLA-DQ positive. This aberrant major histocompatibility complex class II antigen expression in smooth muscle and endothelial cells may participate in the perpetuation of the atherogenetic autoimmune reaction.

Adolescent↗
PubMed1992

Accelerated decay of the cell bound C4b2a complex by serum of patients with membranoproliferative glomerulonephritis and acute poststreptococcal glomerulonephritis.

Serum from patients with membranoproliferative glomerulonephritis (MPGN) and acute poststreptococcal glomerulonephritis (APSGN) accelerated the decay of the cell bound C4b2a (C42) and C4b hemolytic activity relative to pooled normal human serum (pNHS) after 5 min incubation at 30 degrees C in EDTA-GVB. The accelerated decay of the C42 hemolytic activity was heat stable (56 degrees C 30 min) and was inhibited by monoclonal antibody against human C4 binding protein (MoAb:C4BP) or C4 binding protein (C4BP) depleted serum. C4 nephritic factor (C4NeF) was employed to stabilize the labile classical pathway C3 convertase C42 complex. Serum from patients with MPGN and APSGN reduced the C4NeF stabilizing activity. Sera from 32 of 46 patients with MPGN and all of 7 patients with APSGN reduced the C42 hemolytic activity relative to 50 normal human serum (NHS) after 5 min incubation at 30 degrees C in EDTA-GVB, and there was no relationship with the serum concentration of C4BP. In vivo, accelerated decay of C42 convertase might interfere with the clearing and processing mechanism of circulating immune complexes (IC) by reducing deposition of C3b on the IC lattice.

Acute Disease↗
PubMed1993

Eosinophil major basic protein enhances the expression of neutrophil CR3 and p150,95.

BACKGROUND: We examined the effect of major basic protein (MBP) stimulation on the expression of the neutrophil B2-integrins: LFA-1 (CD11a/CD18), CR3 (CD11b/CD18), and p150,95 (CD11c/CD18). METHODS: Incubation of neutrophils with 0.75 to 3.0 mumol/L MBP for 30 minutes at 37 degrees C resulted in concentration-dependent increases in CR3 expression as detected by staining with the CD11b-specific monoclonal antibody, Leu-15. RESULTS: The expression of CR3 was significantly (p < 0.001) higher when neutrophils were stimulated with 1.5 mumol/L (53% +/- 9% increase) or 3.0 mumol/L (100% +/- 17% increase) MBP as compared with unstimulated neutrophils. The kinetics of MBP-stimulated CR3 expression were rapid and were similar to those of 100 nmol/L. N-formyl-methionyl-leucyl-phenylalanine-stimulated enhancement of CR3 expression. Incubation of neutrophils with reduced and alkylated MBP resulted in significantly lower (p < 0.05) increases in CR3 expression as compared with stimulation with native MBP. In addition, neither eosinophil cationic protein nor eosinophil-derived neurotoxin altered neutrophil CR3 expression. MBP stimulated minimal increases in LFA-1 expression. However, staining with the monoclonal antibody Leu-M5 (anti-CD11c) revealed that MBP stimulated significant increases in the expression of p150,95. CONCLUSIONS: These results indicate that MBP stimulates the increased expression of neutrophil adhesion molecules, which in turn may enhance the inflammatory role of neutrophils in the late-phase events of allergic diseases.

Blood Proteins↗