bluuebunny/crossref_metadata_2025_split huggingface dataset:
The IgE and IgG antibody responses to aerosols of Nephrops norvegicus (prawn) antigens: the association with clinical hypersensitivity and with cigarette smoking
Authors: McSHARRY C , ANDERSON K , McKAY I C , COLLOFF M J , FEYERABEND C , WILSON R B , WILKINSON P C 
Published: July 2010

SUMMARY
Raised levels of serum IgE antibodies to prawn antigens were found in 15 of 26 seafood factory process workers with respiratory symptoms and in one of 26 case-matched asymptomatic controls (P &lt; 0.001). Raised IgG antibody titres against the same antigens were found in 18 subjects in each symptom grouping, and the median titres of this antibody did not differ significantly between the groups. The prawn-specific IgE antibody response was significantly associated with atopy (IgE antibody response to common allergens) and with a history of cigarette smoking, confirmed by level of serum cotinine, a major nicotine metabolite. Non-atopic non-smokers were unlikely to become sensitized. The titre of the prawn-specific IgE antibody correlated with the duration of exposure and with the duration of symptoms. Discriminant analysis of the serological profile (anti-prawn IgE, total IgE and cotinine) was sufficient to assign individuals correctly into symptomatic or asymptomatic categories in 77% of subjects. The titres of the IgE and IgG antibody responses to prawn antigens did not correlate, and the main factor which seemed to determine the antibody isotype response to these inhaled antigens was cigarette smoking. IgE antibody was produced mainly by smokers, whereas IgG antibody was the predominant isotype produced by non-smokers.
Increase in the proportion of granulated CD56+ T cells in patients with malignancy
Authors: TAKII Y , HASHIMOTO S , IIAI T , WATANABE H , HATAKEYAMA K , ABO T 
Published: July 2010

SUMMARYEvidence is presented for the existence of a unique T cell population which expressed one of the natural killer (NK) markers, CD56 antigen, in humans. Although such 0056+ T cells were a minor population in the peripheral blood (&lt; 10%). They were abundant in the liver (up to 50%). which was recently demonstrated to be a major organ for extrathymic T cell differentiation in mice. As in the case of extrathymic T cells in mice, these CD56+ T cells in humans contained a higher proportion of γδ cells than did CD56− T cells, contained double-negative CD4−8 cells, and had the morphology of large granular lymphocytes. This unique population of CD56+ T cells tended to be elevated in the blood and among tumour-infiltrating lymphocytes in patients with colorectal cancer, especially in advanced cases. These results raise the possibility that, as in mice, CD56+ T cells with extrathymic T cell properties may also be associated with tumour immunity in humans.
HIV-1 recombinant gp160 vaccine given in accelerated dose schedules
Authors: GORSE G J , SCHWARTZ D H , GRAHAM B S , MATTHEWS T J , STABLEIN D M , FREY S E , BELSHE R B , CLEMENTS M L , WRIGHT P F , EIBL M , FAST P E 
Published: July 2010

SUMMARY
The purpose of this randomized, double-blind study was to test the safely and immunogenicity of an HIV-ILAI recombinant gp160 (rgp160) vaccine in healthy, uninfected volunteers using accelerated dosing schedules. Thirty volunteers were randomly assigned lo receive 50μg doses of rgp160 in one of two immunization schedules. Group 1 received rgp160 at times 0, 1, 2 and 5 months: and group 2 received rgp160 at times 0, 1, 2, 3 and 4 months. The vaccine was safe and stimulated high levels of HIV-1 envelope-specific binding antibody and T cell memory. There was a trend (P &lt; 0.10) suggesting neutralizing antibodies were better induced by the regimen incorporating a rest period before the final immunization in group 1 volunteers. Both accelerated immunization schedules induced immune responses at levels similar to or better than those achieved by four rgp160 vaccine injections given over 12-18 months in other studies.
Interactions between murine AIDS (MAIDS) and toxoplasmosis in co-infected mice
Authors: LACROIX C , LEVACHER-CLERGEOT M , CHAU E , SUMUYEN M H , SINET M , POCIDALO J J , DEROUIN F 
Published: July 2010

SUMMARYWe coinfected C57B1/6 mice with LP-BM5 murine leukaemia viruses, responsible for murine AIDS (MAIDS), and an avirulent strain of Toxoplasma gondii. Virus-infected mice were infected perorally on day 30 with 10 cysts of T. gondii, and T. gondii-infected mice were challenged with LP-BM5 on day 20, 30 or 60 after parasite inoculation. Uninfected and singly infected mice were used as controls. The kinetics of parasite burden in blood, lungs and brain, together with blood lymphocyte subsets, and spleen and lymph node weights, were serially determined in each group of mice. The kinetics of parasite counts in mice infected by LP-BM5 then by T. gondii were similar to those in mice infected by T. gondii only except for lung counts, which reached higher values than in animals infected with T. gondii alone, then fell and re-increased until the end of the experiment. The only significant change in parasite burdens when mice were first infected by T. gondii and then by LP-BM5, compared with T. gondii controls, was an increase in lung counts in mice challenged with LP-BM5 20 days after T. gondii inoculation. Whatever the schedule of co-infection, the kinetics of lymphocyte subsets in co-infected mice differed from those in T. gondii-or LP-BM5-infected mice; in dually infected mice CD4+ and CD8+ cell counts were intermediate between values in mice singly infected by the parasite or the virus. Enlargement of spleen and lymph nodes, which is a major criterion of MAIDS progression, was significantly less marked in co-infected mice than in mice infected with LP-BM5 alone. These data point to cross-regulation of T. gondii and LP-BM5 infections, which results in increased susceptibility to T. gondii and may alter the progression of MAIDS.
Effects of 17β-oestradiol on function of lymphocytes from normal donors and patients with common variable immunodeficiency (CVID)
Authors: EVAGELATOU M , WEBSTER A D B , FARRANT J 
Published: July 2010

SUMMARYEffects of oestradiol (E2) have been studied on the in vitro T cell-dependent differentiation of B cells from peripheral blood and spleen using normal donors and patients with the antibody deficiency disease CVID. We also studied whether it modifies T cell DNA synthesis. The effect of E2 was examined on cultures of B cells with T cells for IL-2-driven immunoglobulin secretion or of T cells for phytohaemagglutinin (PHA)-driven DNA synthesis. Interestingly, in control experiments without E2, the normal sex difference in immunoglobulin production is reversed in CVID. The data show that for normal individuals there is no major difference between male and female donors in the in vitro actions of E2 on blood B and T lymphocytes. With normal blood B cells, E, failed to affect IgM production, but it did inhibit IgG. In normal splenic cells, E2 increased both IgM and IgG secretion in a similar way to the tonsillar cell data previously reported. E2 on normal blood T cell DNA synthesis was stimulatory. With blood cells from CVID patients an interesting contrast was seen. As with normal B cells, E2 had no effect on IgM secretion by those CVID blood B cells able to secrete IgM. However, a difference between patients and normals was that E2 did not inhibit the IL-2-driven IgG production by those CVID B cells able to secrete IgG. For T cell function, the stimulatory effect of E2 on CVID T cell DNA was as in normal T cells. However, E2 failed to restore CVID B and T cell function to normal levels. These data suggest that there may be subtle defects in the pathway of action of E2 in CVID lymphocytes.
Characterization of the virulence of Mycobacterium avium complex (MAC) isolates in mice
Authors: PEDROSA J , FLÓRIDO M , KUNZE Z M , CASTRO A G , PORTAELS F , McFADDEN J , SILVA M T , APPELBERG R 
Published: July 2010

SUMMARY
The virulence of different isolates of MAC was studied in naturally susceptible BALB/c mice. In preliminary experiments, MAC bacteria forming smooth transparent colonies on solid media (SmT variants) were found to be virulent for BALB/c mice, causing progressive infection; smooth opaque (SmOp) were generally avirulent, being slowly eliminated from the infected organs; and rough (Rg) variants were either avirulent or as virulent as SmT variants. We chose to compare the virulence of different isolates of MAC of different origins, studying only the SmT morphotype. Strains of MAC isolated from naturally infected animals were those that most consistently caused progressive infections. AIDS patients-derived isolates were of intermediate virulence or devoid of virulence in mice. The environmental strains were eliminated from mice or did not proliferate. Strains of MAC isolated from individuals who were not infected by HIV varied in virulence from completely avirulent to highly virulent. There was no close correlation between virulence and restriction fragment length polymorphism (RELP) type, although all highly virulent strains were of the A/I type. There was also no correlation between virulence analysed in vivo and the ability to grow in cultured macrophages.
Heat shock proteins as carrier molecules:in vivohelper effect mediated byEscherichia coliGroEL and DnaK proteins requires cross-linking with antigen
Authors: BARRIOS C , GEORGOPOULOS C , LAMBERT P-H , DEL GIUDICE G 
Published: July 2010

SUMMARYIn the past few years we have shown that mycobacterial heat shock proteins (hsp) of 65 and 70 kD exert a very strong helper effect in mice and monkeys when conjugated to peptides and oligosaccharides and given in the absence of adjuvants. In the present study we show that this adjuvant-free helper effect (1) is not due to lipopolysaccharide (LPS), since it was observed in LPS-resistant mice (C3H/HeJ) immunized with hsp-based constructs containing the malaria peptide (NANP)40, and (ii) is characteristic of hsp, since it was not observed with conjugates containing the mycobacterial p38 antigen, which is not a stress protein. Interestingly, the hsp GroEL and DnaK of Escherichia coli, which share a high degree of homology with the mycobacterial 65-kD and 70-kD hsp respectively, exhibit a strong in vivo helper effect when conjugated to the (NANP) peptide and the conjugates given in the absence of adjuvants. This in vivo helper behaviour of the GroEL and DnaK proteins corresponds well to that observed with the mycobacterial 65-kD and 70-kD hsp. respectively, since the hsp65- and GroEL-based constructs require previous priming of the animals with live bacille Calmette Guérin (BCG), which is not needed for the hsp70- and DnaK-based constructs. Finally, using both mycobacterial and E. coli hsp we show that their in vivo helper effect in the absence of adjuvants requires cross-linking to the synthetic peptide. Taken together, our results suggest that the adjuvant-free helper effect observed with mycobacterial and E. coli hsp may be a generalized phenomenon, exhibited by hsp from diverse microorganisms. These findings may find applications in the design of vaccine constructs.
Soluble endothelium-associated adhesion molecules in patients with Graves' disease
Authors: WENISCH C , MYSKIW D , PARSCHALK B , HARTMANN T , DAM K , GRANINGER W 
Published: July 2010

SUMMARYThe targeting and recruitment of inflammatory cells to vascular endothelium in Graves' disease (GD) is mediated by intercellular adhesion molecule-1 (ICAM-1), endothelial leucocyte adhesion molecule-1 (ELAM-1), and vascular cell adhesion molecule-1 (VCAM-1). We have studied serum levels of soluble ICAM-1 (sICAM-1), soluble ELAM-1 (sELAM-1), and soluble VCAM-1 (sVCAM-1) in patients with GD (n= 21) and in patients with iodine-deficient goitre (IDG) (n= 23). The serum levels of sICAM-1 were markedly elevated in patients with GD before treatment with thiamazole (median 560 ng/ml versus 185 ng/ml in patients with IDG). In addition, elevated serum concentrations of sELAM-1 (median 85 ng/ml versus 33 ng/ml, respectively) and sVCAM-1 (median 42 ng/ml versus 15 ng/ml, respectively) were observed in patients with GD (P &lt; 001 for all). The serum levels of sELAM-1 and sVCAM-1 dropped significantly after initiation of therapy and were within the normal range after 4, and 8 weeks of therapy, respectively. Serum levels of sICAM-1 were elevated even after 8 weeks of therapy. Serum levels of sVACM-1 and sICAM-1 correlated with the serum concentrations of anti-thyroid-stimulating hormone (TSH)-receptor antibodies (TSHR-R) (n= 21; r= 0929 and r= 0810, respectively) and anti-thyroid peroxidase antibodies (TPO-Ab) (n= 21; t=0-673 and r= 0-750, respectively). However, no correlation between sELAM-1 and TPO-Ab, TSHR-R, and anti-thyroglobulin antibodies (Tg-Ab), respectively, could be found. In addition to thyroid hormones and autoantibodies, serum concentrations of sELAM-1 and sVCAM-1, but not sICAM-1, could be useful as clinical markers for disease activity.
Activation of granulocytes by anti-neutrophil cytoplasmic antibodies (ANCA): a FcγRII-dependent process
Authors: MULDER A H L , HEERINGA P , BROUWER H , LIMBURG P C , KALEENBERG C G M 
Published: July 2010

SUMMARYANCA have been demonstrated to induce the respiratory burst in primed neutrophils. In this study we have extended the investigations on neutrophil activation by ANCA directed against proteinase 3 (PR3). Myeloperoxidase (MPO) and lactoferrin (LF), and we have analysed the underlying mechanisms. All three ANCA antigens were expressed on the cell surface of primed neutrophils. Superoxide production assayed by both cytochrome c reduction and oxidation of dihydrorhodamine 123, was induced by heterologous polyclonal anti-MPO and anti-LF antibodies, and ANCA-positive plasma samples. Induction of superoxide production was dose-dependent. F(ab)2 fragments did not induce the respiratory burst. Blockade of Fc receptors by specific oAbs showed that anti-FcγRII antibodies were able to turn off the ANCA-induced respiratory burst, whereas anti-FcγRII antibodies did not. Plasma samples that induced the respiratory bursl did not differ from samples that did not induce superoxide production with respect to ANCA titre, but had higher levels of the lgG3 subclass of ANCA. Levels of the other subclasses of ANCA were comparable between those samples. We conclude that ANCA-induced activation of primed neutrophils is FcγRII-dependent, and appears to be facilitated by antibodies of the IgG3 subclass.
Antibodies to DNA, chromatin core particles and histones in mice with graft-versus-host disease and their involvement in glomerular injury
Authors: MEZIERE C , STOCKL F , BATSFORD S , VOGT A , MULLER S 
Published: July 2010

SUMMARYChronic graft-versus-host disease (GVHD) was induced in female (C57 B10S/DBA/2)F1 hybrid mice with two successive injections of lymphoid cells from parental DBA/2 strain. Serial bleedings of 27 GVHD mice were screened with a panel of antigens including the five histones HI, H2A, H2B, H3 and H4, 15 histonc peptides. core particles. dsDNA. heat-shock proteins hsp70 and ubiquitin, a branched peptide of ubiquitinaled H2A (U-H2A), poly(ADP-ribose) and SSB/La protein. The predominant IgG response to histone peptides was directed against regions 204-218 of HI, 1-25 of H2B and 1 29 of H4. GVHD mice also produced IgG antibodies lo dsDNA and chromatin core particles as reported previously. IgG antibodies reacting with dsDNA appeared before antibodies to core particles and histones. Raised levels of antibodies to U-H2A, but not to monomeric ubiquitin, were also found. While the level of antibodies to dsDNA, histones and core particles decreased significantly before the appearance of proteinuria, suggesting their involvement in glomerular injury, the longitudinal pattern of anti-U-H2A peptide response was apparently not linked to the manifestation of lupus nephritis in GVHD mice.
Intercellular adhesion molecule-1 (ICAM-1) expression and soluble ICAM-1 (sICAM-1) production by cytokine-activated human aortic endothelial cells: a possible role for ICAM-1 and sICAM-1 in atherosclerotic aortic aneurysms
Authors: SZEKANECZ Z , SHAH M R , PEARCE W H , KOCH A E 
Published: July 2010

SUMMARYThe interactions of inflammatory cells, cytokines, and cell adhesion molecules (CAM) may be important in the pathogenesis of vascular diseases such as abdominal aortic aneurysms (AAA), in which inflammation plays a role. The aim of this study was to investigate the pathogenic role of ICAM-1, a molecule involved in leucocyte-endothelial interactions, in vascular inflammation. ELISA of human explant culture supernatants revealed a four-fold increase in sICAM-1 production by AAA (n = 9) versus normal (n = 8) aortic explants. Human aortic endothelial cell (hAEC) culture was used for further studies as an in vitro model for aortic inflammatory conditions. Tumour necrosis factor-alpha (TNF-α) or IL-β treatment of hAEC resulted in an up to 1-8-fold significant increase in sICAM-1 production compared with resting cells. In addition, the expression of ICAM-1 on cytokine-stimulated versus resting hAEC was measured by radioimmunoassay. TNF-α significantly induced ICAM-1 expression on these cells. These results suggest that different forms of ICAM-1, present on or released by the activated aortic endothelium, may be involved in leucocyte adhesion to and migration into the vessel wall.
Histamine induces IL-6 production by human endothelial cells
Authors: DELNESTE Y , LASSALLE P , JEANNIN P , JOSEPH M , TONNEL A B , GOSSET P 
Published: July 2010

SUMMARYHistamine is one of the major mediators implicated in the physiopathology of allergy. On vascular endothelium, histamine mainly induces early effects: an increase in vasopermeability leading to oedema, a release of lipid mediators and a transient expression of P-selectin. The aim of this study was to evaluate the effects of histamine on adhesion molecule expression and IL-6 production by human endothelial cells. Histamine did not modulate the expression of intercellular adhesion molecule-1 (ICAM-1). vascular cell adhesion molecule-1 (VCAM-1) and E-selectin but induced a transient expression of P-selectin as previously reported. In addition, histamine increased in a dose-(from 10−5 to 10−3 M) and time- (from 4h to 24 h) dependent fashion the IL-6 synthesis by endothelial cells. Tumour necrosis factor-alpha (TNE-α)-induced IL-6 production was also potentiated in a dose-dependent manner by histamine, without modification of the time course of IL-6 secretion. Moreover, this increase of IL-6 production induced by histamine was inhibited in a dose-dependent manner by HI and H2 histamine receptor antagonists (50% inhibition of IL-6 production at 5 × 10−4M and 4 × 10−5 M, respectively). So histamine induces, besides already well known effects, a late stimulation of endothelial cells, i.e. the production of IL-6.
Elevated levels of soluble CD 14 in serum of patients with systemic lupus erythematosus
Authors: NOCKHER W A , WIGAND R , SCHOEPPE W , SCHERBERICH J E 
Published: July 2010

SUMMARYA soluble form of CD14 (sCD14) was assessed with an ELISA assay in the serum of the following three clinical groups: 35 patients with an inactive phase of systemic lupus erythematosus (SLE). 17 patients with SLE relapses, and 65 normal healthy volunteers, Increased levels of sCD14 were observed in all patients suffering from SLE compared with normal controls. In addition, patients with active SLE revealed higher serum concentrations of sCD14 (median 6·9 mg/l) than patients under remission (4·1 mg/l; P&lt; 0·0001). Serum values of sCD14 correlated neither with the number of peripheral blood monocytes bearing the CD 14 membrane antigen, nor with serum concentrations of IL-1β. Serum sCD14 was compared with other clinical parameters used to monitor the clinical course of patients with SLE, among them complement C3. anti-dsDNA antibodies and soluble IL-2 receptor (sIL-2R). A good correlation emerged between sCD14 and C3 as well as sIL-2R concentrations. but sCD14 and anti-dsDNA titres disclosed no significant correlation in both groups of patients with SLE. Serial studies in patients with severe SLE showed that serum sCD14 closely parallels the clinical course as defined by an activity score. Our data suggest that serum sCD14 represents a promising parameter lo monitor disease activity in patients with SLE.
Experimental arthritis induced by continuous infusion of IL-8 into rabbit knee joints
Authors: ENDO H , AKAHOSHI T , NISHIMURA A , TONEGAWA M , TAKAGISHI K , KASHIWAZAKI S , MATSUSHIMA K , KONDO H 
Published: July 2010

SUMMARYTo determine the roles of IL-8 in inflammatory synovitis. examination was made of the results of continuously injecting human recombinant IL-8 into the knee joints of New Zealand white rabbits. Recombinant human lL-8 was infused continuously into the joint cavity at 75 ng/h for 14 days by a polypropylene catheter connected to a mini-osmotic pump implanted in each rabbit. Infiltration of inflammatory cells into joint cavity and histopathological changes in synovial tissue were examined at 7 and 14 days following the start of infusion. The continuous infusion of IL-8 for 14days led to severe arthritis characterized by apparent erythema and joint pain, the accumulation of leucocytes, infiltration of mononuclear cells in synovial tissue, and marked hypervascularization in the synovial lining layer. IL-8 may be a factor which can contribute to the inflammatory process of chronic arthritis by mediating leucocyte recruitment and hypervascularization in inflamed joints.
Impaired granulocyte oxidative burst and decreased expression of leucocyte adhesion molecule-1 (LAM-1) in patients with Wegener's granulomatosis
Authors: RIECKEN B , GUTFLEISCH J , SCHLESIER M , PETER H H 
Published: July 2010

SUMMARY
Neutrophils are the target of autoantibodies in Wegener's granulomatosis (WG). In this study, granulocyte function and surface marker expression were investigated in patients with WG. The oxidative burst in response to phorbol myristate acetate (PMA) was tested with granulocytes of 25 patients with histologically proven WG. A significantly diminished percentage of oxygen radical-producing cells was found in patients with active disease. Surface antigen expression of CD 11 b and LAM-1 was analysed on granulocytes of 20 patients with WG. Whereas the expression of CD 11 b was normal, surface expression of LAM-1 was decreased in nine cases with WG. The decrease of LAM-1 correlated with disease activity. Phagocytosis of Escherichia coli was tested in 10 patients with WG, and normal values were found in all cases. We conclude that down-regulation of LAM-1 may be a marker of disease activity in WG. The altered response to PMA may indicate functional changes in granulocyte reactivity due to autoantibody-induced damage of the granulocyte membrane.