bluuebunny/crossref_metadata_2025_split huggingface dataset:
T and IgA B Lymphocytes of the Pharyngeal and Palatine Tonsils: Differential Expression of Adhesion Molecules and Chemokines
Authors: Bourges D. , Wang C. H. , Chevaleyre C. , Salmon H. 
Published: September 2004

AbstractThe pharyngeal (Ph) and palatine (Pa) tonsils, although located in different regions of the upper aero‐digestive tract (UADT), are thought to protect the respiratory tract similarly against infections by inducing and disseminating T and surface IgA+ (sIgA+) B cells. We investigated the factors controlling the migratory properties of T and sIgA+ B lymphocytes in the UADT of pigs by comparing the expression of vascular addressins, homing receptors and chemokine transcripts in Ph/Pa tonsils, Peyer's patches (PP) and their draining lymph nodes (LN). The vascular addressin PNAd was detected on high endothelial venules in both tonsils, whereas mucosal addressin cell adhesion molecule‐1, otherwise present in PP and mesenteric LN, was not detected. More importantly, the vascular cell adhesion molecule‐1 (VCAM‐1) addressin was present in Ph tonsil and LN but neither in Pa tonsil nor in PP vascular cells, whereas both T and sIgA+ B lymphocytes displayed similar levels of α4β1high integrin, the ligand of VCAM‐1. Analysis of transcript levels for several lymphoid (CCL19, CXCL12 and CCL21) and epithelial chemokines also demonstrated opposite chemokine mRNA ratios for Ph tonsil (CCL28 > CCL25) and PP, with Pa tonsil expressing very low levels of CCL28. Collectively, these data indicate that the differential compartmentalization of sIgA+ lymphocytes between Pa and Ph tonsils may partly result from the differential expression of VCAM‐1 and CCL28. They also suggest that tonsillar addressins and epithelial chemokines, rather than the cells intravasating it, control the regionalization of sIgA+ lymphocytes in the UADT.
Dose‐dependent Immunomodulatory Effects of Acetylsalicylic Acid and Indomethacin in Human Whole Blood: Potential Role of Cyclooxygenase‐2 Inhibition
Authors: Härtel C. , Von Puttkamer J. , Gallner F. , Strunk T. , Schultz C. 
Published: September 2004

AbstractThe aim of the study was to characterize the in vitro effect of non‐steroidal anti‐inflammatory drugs (NSAIDs) on the production of pro‐inflammatory cytokines in a human whole blood assay. Whole blood samples were pre‐incubated with acetylsalicylic acid, indomethacin, selective cyclooxygenase (COX)‐1 inhibitor (SC‐560), COX‐2 inhibitor (NS‐398) or prostaglandin E2 (PGE2) before stimulation with lipopolysaccharide (LPS). Pro‐inflammatory and anti‐inflammatory cytokines were determined directly at the cell level with the help of flow cytometry and/or in the plasma supernatant with the help of ELISA. High doses of acetylsalicylic acid were needed to inhibit pro‐inflammatory cytokine production. In contrast, low‐to‐moderate doses induced a modestly enhanced production of pro‐inflammatory cytokines. Moreover, indomethacin was demonstrated to increase the expression of interleukin‐6 (IL‐6) and tumour necrosis factor‐α (TNF‐α) in a dose‐dependent fashion. Upon addition of PGE2, however, LPS‐induced IL‐6 and TNF‐α production was suppressed regardless of indomethacin presence. Interestingly, selective COX‐2 inhibition (NS‐398), but not selective COX‐1 inhibition (SC‐560), exerted a stimulatory effect on the expression of pro‐inflammatory cytokines. These data emphasize that the immunomodulating effects of NSAIDs in whole blood are dose‐dependent. Furthermore, the induction of pro‐inflammatory cytokine expression by NSAIDs is potentially mediated by COX‐2 inhibition. Although NSAIDs are successfully used in clinical practice for their net anti‐inflammatory properties, our observations may contribute to the understanding of side effects induced by NSAIDs and selective COX‐2 inhibitors.
Abnormal Cell‐Specific Expressions of Certain Protein Kinase C Isoenzymes in Peripheral Mononuclear Cells of Patients with Systemic Lupus Erythematosus: Effect of Corticosteroid Application
Authors: Bíró T. , Griger Z. , Kiss E. , Papp H. , Aleksza M. , Kovács I. , Zeher M. , Bodolay E. , Csépány T. , Szûcs K. , Gergely P. , Kovács L. , Szegedi G. , Sipka S. 
Published: September 2004

AbstractWe have studied the expressions of various protein kinase C (PKC) isoenzymes in T cells and monocytes from patients with systemic lupus erythematosus (SLE), in comparison to those of healthy controls and patients with other immunological disorders. As measured by Western blotting, the levels of PKCβ, δ, η, ε, θ and ζ (but not of PKCα) significantly decreased in T cells of SLE patients. In monocytes, however, we observed marked suppressions only in the expressions of PKCδ, ε and ζ but not in the expressions of other PKC isoforms. In vivo corticosteroid application, as well as in vitro steroid treatment of monocytes, elevated the expressions of most isoforms close to normal values; however, the decreased levels of PKCθ and ζ were not affected by steroid application. These alterations were characteristic to SLE because we could not detect any changes in the PKC levels in mononuclear cells of primary Sjögren's syndrome and mixed connective tissue disease patients. These results suggest that impaired PKC isoenzyme pattern may exist in the T cells and monocytes of SLE patients. Furthermore, the clinically efficient glucocorticoid application in SLE can increase the expression of some members of PKC system.
Long‐Distance Running Modulates the Expression of Leucocyte and Endothelial Adhesion Molecules
Authors: Nielsen H. G. , Lyberg T. 
Published: September 2004

AbstractThere still exist many unanswered questions whether physical exercise is beneficial or harmful to the immune system. The ‘open‐window’ post‐exercise hypothesis states that athletes are more susceptible to infections after exercise, but there is a need for further elucidation. The aim of the present study was to investigate the effect of long‐distance running on leucocyte expression of selected adhesion molecules as well as the plasma levels of soluble leucocyte‐ and endothelium‐derived adhesion molecules. Twenty‐seven men participating in Oslo marathon together with 16 entrants (eight men and eight women) in the Oslo half‐marathon were recruited to this study. Venous blood was collected before and immediately after the races for analysing the leucocyte expression of CD62L, CD11b and CD14 with the help of flow cytometry, and plasma concentrations of soluble (s) sE‐selectin, sL‐selectin, sP‐selectin, sVCAM‐1, sICAM‐1 and sCD14 were assessed by means of enzyme‐linked immunosorbent assays. A significant increase of leucocyte CD11b expression was observed following both races, compared to the pre‐race situation. Monocyte CD14 expression increased only after the marathon race. After both races, CD62L expression was significantly lowered on all leucocyte subsets, whereas the plasma levels of sE‐selectin, sP‐selectin, sL‐selectin, sVCAM‐1, sICAM‐1 and sCD14 were all increased. Altogether, these changes negatively influence the ability of leucocytes to adhere to and actively transmigrate the endothelium to reach the tissues. Our study thus supports the ‘open‐window’ hypothesis, indicating a reduced capacity to combat infectious agents during the immediate post‐exercise period.
Mammalian Cell‐Entry Proteins Encoded by the mce3 Operon of Mycobacterium tuberculosis are Expressed During Natural Infection in Humans
Authors: Ahmad S. , El‐Shazly S. , Mustafa A. S. , Al‐Attiyah R. 
Published: September 2004

AbstractThe mammalian cell‐entry (mce)3 operon is one of four homologous mce operons on Mycobacterium tuberculosis genome that encodes six putative invasin/ adhesin‐like proteins (Mce3A–F) possibly involved in the entry and survival of this bacterium inside macrophages. To study the in vivo expression of the mce3 operon‐encoded proteins during natural human infection, the genes encoding Mce3A–F were cloned and expressed in Escherichia coli as fusion proteins with glutathione‐S‐transferase (GST) at the N‐terminal and a ×6 histidine (His) tag at the C‐terminal end. The recombinant proteins appeared as major cellular proteins in SDS‐PAGE gels and reacted with anti‐GST and antipenta‐His antibodies at the expected molecular mass of 72, 61, 78, 80, 66 and 78 kDa for GST‐Mce3A, GST‐Mce3B, GST‐Mce3C, GST‐Mce3D, GST‐Mce3E and GST‐Mce3F, respectively. In Western immunoblots, all the six fusion proteins, particularly GST‐Mce3A, GST‐Mce3C, GST‐Mce3D and GST‐Mce3E, reacted with antibodies in combined human serum from 11 tuberculosis (TB) patients. Pure Mce3A, Mce3D and Mce3E could be isolated by specific proteolytic cleavage by thrombin protease of the respective purified fusion protein followed by preparative SDS‐PAGE. The pure Mce3A, Mce3D and Mce3E reacted to various extents with antibodies in serum samples from TB patients. The Mce3E reacted with 51 of 55 (93%) and all the three proteins reacted with 34 of 55 (62%) serum samples. The Mce3A, Mce3D and Mce3E proteins also reacted, albeit at lower frequency, with one of 23 (4%) serum sample obtained from M. bovis bacillus Calmette–Guérin‐vaccinated healthy subjects and four of 18 (22%) serum samples from long‐term contacts of TB patients showing reactivity with all the three Mce3 proteins. The data show that Mce3A, Mce3D and Mce3E encoded by mce3 operon of M. tuberculosis are expressed and elicit antibody responses in humans during natural infection with this pathogen.
Hydrostatic Pressure Induces Apoptosis in the Human Leukaemic T‐Cell Line Jurkat Via the Mitochondrial Pathway
Authors: Klett M. V. , Boneberg E.‐M. , Trenz K. , Knippers R. , Illges H. 
Published: September 2004

AbstractWe investigated the effect of pressure levels ranging from 80 to 500 bar on the proliferative capacity and viability of Jurkat leukaemic T cells. Pressurization at 360 bar induced apoptotic cell death as shown by apoptotic morphology after Hoechst staining, DNA fragmentation in the TdT‐mediated dUTP nick end labelling‐assay and cleavage of several caspase substrates. Cell death could be prevented by the general caspase inhibitor zVAD‐fmk. Breakdown of the mitochondrial membrane potential and the release of cytochrome c provided strong evidence for an involvement of the mitochondrial pathway, whereas a central role of the death receptor pathway was excluded because caspase‐8 was not significantly activated. Pressure incubation led to calcium influx after 5 min, and we hypothesize that calcium influx could be the primary trigger for pressure‐induced apoptosis.
Immunogenicity and Vaccine Potential of Dipeptidic Multiple Antigen Peptides from Schistosoma mansoni Glyceraldehyde 3‐Phosphate Dehydrogenase
Authors: El Ridi R. , Montash M. , Tallima H. 
Published: September 2004

AbstractSix peptides, A, B1, B, C, D and E, derived from the primary sequence of Schistosoma mansoni glyceraldehyde 3‐phosphate dehydrogenase (SG3PDH) were selected based on lowest homology to human glyceraldehyde 3‐P dehydrogenase (G3PDH), multimerized in dipeptidic multiple antigen peptide (D‐MAP) constructs and used for the immunization of BALB/c mice. Tetrabranched D‐MAPs A–B, B1–C and D–E and the bis‐D‐MAP B–E elicited strong cell‐mediated and antibody responses against immunogen, unit peptides and their cognate sequences in the native and denatured protein. D‐MAP A–B induced protection against challenge infection. Immunization with D‐MAP B1–C failed to affect the challenge worm parameters, probably because peptides B1 and C, previously shown to elicit immune responses associated with increase and decrease in challenge worm fertility, respectively, induced immune responses with opposing effects when combined in a D‐MAP construct. A similar suggestion may explain the failure of D‐MAP D–E to protect the host against challenge infection. In contrast, immunization with D‐MAP B–E resulted in robust protection of the host, possibly because it contains peptides known to evoke immune responses associated with a significant decrease in challenge worm burden and fertility. The data together suggest that the specificity, not the quantity, of the induced immune responses is the determining factor for the efficacy of synthetic peptide‐based vaccine for schistosomiasis.
Production of Heymann nephritis by a chemically modified renal antigen
Authors: Barabas Arpad Z. , Cole Chad D. , Barabas Arpad D. , Lafreniere Rene 
Published: September 2004

SummaryAn autoimmune kidney disease morphologically and functionally similar to Heymann nephritis (HN) was induced in mature male Sprague Dawley rats by repeated weekly IP injections of a chemically modified azo sonicated ultracentrifuged (u/c) rat kidney fraction 3 (rKF3) antigen in an aqueous medium. The experiment was terminated 15 weeks after the first injection of the chemically altered antigen. Serum samples collected and analysed by an indirect fluorescent antibody test on normal rat kidney sections during the course of the experiment showed a gradual rise in circulating pathogenic autoantibodies directed against the proximal tubular brush border regions. Proteinuria was present and significantly increased in the urine of two of eight rats. The arising immune‐complex glomerulonephritis (ICGN) revealed typical HN kidney disease lesions in 70% of the rats in histological, direct fluorescent antibody and electron‐microscopical examinations. Control rats injected similarly with the an unmodified version of the same antigen did not develop the HN‐characteristic morphological and functional changes. To our knowledge, this is the first time that the autoimmune kidney disease designated as an active HN has been produced by the administration of a chemically altered renal antigen in an aqueous solution and not by the usual presentation of the nephritogenic renal antigen in an adjuvant.
The effects of coadministration of dietary copper and zinc supplements on atherosclerosis, antioxidant enzymes and indices of lipid peroxidation in the cholesterol‐fed rabbit
Authors: Alissa Eman M. , Bahijri Suhad M. , Lamb David J. , Ferns Gordon A. A. 
Published: September 2004

SummaryIt has previously been shown that dietary copper can modulate the extent of atherosclerosis in the thoracic aorta of cholesterol‐fed rabbits. The metabolism of copper and zinc are closely related, and it has been hypothesized that the balance of dietary copper to zinc may be important in determining coronary risk. Hence, we have investigated the interaction between dietary copper and zinc in atherogenesis in the New Zealand White rabbit. Juvenile male rabbits were randomly allocated to eight groups. Four groups were fed a normal chow diet with zinc (0.5%, w/w), copper (0.2%, w/w), copper plus zinc or neither in their drinking water for 12 weeks. Four other groups were fed a diet containing 0.25–1% (w/w) cholesterol plus zinc, copper, both or neither. Serum cholesterol of individual animals was maintained at approximately 20 mmol/l.Integrated plasma cholesterol levels were similar for all groups receiving cholesterol and significantly higher than those in the chow‐fed groups (P < 0.001). Aortic copper concentrations were higher in the animals receiving cholesterol diets with copper compared to rabbits receiving normal chow and copper (P < 0.001). Aortic zinc content was significantly higher in cholesterol‐fed rabbits supplemented with zinc alone or with copper than in those fed cholesterol alone (P < 0.001). Plasma ceruloplasmin concentrations were significantly higher in groups receiving cholesterol, irrespective of their trace element supplementation (P < 0.001). However, trace element supplementation increased the level significantly (P < 0.05). Trace element supplements did not appear to affect erythrocyte superoxide dismutase in the cholesterol‐fed animals; however, zinc supplementation was associated with a significant increase in the enzyme in chow‐fed animals (P < 0.05). The activity of the enzyme per mg of protein in aortic tissue was higher in animals receiving copper in the presence of cholesterol (P < 0.05) but not significantly so in its absence. Dietary trace element supplementation in cholesterol‐fed animals was associated with a significant reduction in aortic lesion area. Plasma thiobarbituric acid‐reactive substances and FOX concentrations were both significantly higher in the cholesterol‐fed rabbits compared with the animals that fed on a chow diet (P < 0.001), and these were reduced significantly by dietary copper or zinc supplementation (P < 0.001). Hence, dietary supplements of copper or zinc at the doses used both inhibited aortic atherogenesis in the cholesterol‐fed rabbits, although there was no significant additional effect when given in combination.
Current methods for assaying angiogenesisin vitroandin vivo
Authors: Staton Carolyn A. , Stribbling Stephen M. , Tazzyman Simon , Hughes Russell , Brown Nicola J. , Lewis Claire E. 
Published: September 2004

SummaryAngiogenesis, the development of new blood vessels from an existing vasculature, is essential in normal developmental processes and in numerous pathologies, including diabetic retinopathy, psoriasis and tumour growth and metastases. One of the problems faced by angiogenesis researchers has been the difficulty of finding suitable methods for assessing the effects of regulators of the angiogenic response. The ideal assay would be reliable, technically straightforward, easily quantifiable and, most importantly, physiologically relevant. Here, we review the advantages and limitations of the principal assays in use, including those for the proliferation, migration and differentiation of endothelial cellsin vitro, vessel outgrowth from organ cultures andin vivoassays such as sponge implantation, corneal, chamber, zebrafish, chick chorioallantoic membrane (CAM) and tumour angiogenesis models.
Protein metabolism in guanethidine‐treated rats
Authors: Holeček Milan , Bielavská Marcela , Šprongl Luděk 
Published: September 2004

SummaryThe aim of the present study was to evaluate the effect of short‐term adrenergic blockade on the rate of whole‐body protein turnover and leucine oxidation, and on protein synthesis in specific tissues in male rats. Adrenergic blockade was induced by guanethidine (100 mg/kg body weight subcutaneously). The control group was treated with saline. On the second day, the parameters of whole‐body protein and leucine metabolism were evaluated using a primed constant intravenous infusion of L‐[1–14C]leucine. Protein synthesis in tissues was determined on the basis of L‐[1–14C]leucine incorporation. Guanethidine treatment caused a decrease in norepinephrine in skeletal muscle. Whole‐body leucine oxidation and leucine oxidized fraction were higher in guanethidine‐treated rats. There was an insignificant effect of guanethidine on whole‐body proteolysis, protein synthesis and leucine clearance. However, protein balance was negative due to the larger difference between protein synthesis and proteolysis in guanethidine‐treated animals compared to controls. In guanethidine‐treated rats, protein synthesis was higher in the gastrocnemius muscle and in the kidneys and lower in liver and spleen. Changes in the small intestine and colon were insignificant. In addition, a marked decrease in concentration of several amino acids has been observed in the liver, the kidneys and the spleen. It is concluded that adrenergic blockade induced by guanethidine is associated with significant changes in protein metabolism, leucine oxidation and amino acid concentrations in several tissues. The most important consequences of treatment are considered to be a negative effect on protein balance, increased protein turnover in skeletal muscle and kidneys and decreased protein synthesis in the liver and spleen. These changes may also be induced by administration of other sympathetic blocking agents, e.g. in treatment of hypertension.
Geographical and ethnic differences in gastro‐oesophageal reflux disease
Authors: Kang J. Y. 
Published: September 2004

SummaryBackground : Many observers believe that gastro‐oesophageal reflux disease is more common among white individuals compared with Asians and Afro‐Caribbean subjects.Aim : To perform a asystemic review regarding geographical and ethnic factors in the prevalence of reflux symptoms, endoscopic oesophagitis, hiatus hernia and Barrett's oesophagus.Results : Differences in definitions and methodology make comparison between studies difficult. Overall, however, the community prevalence of reflux symptoms, as well as the prevalence of endoscopic oesophagitis, hiatus hernia and Barrett's oesophagus among patients undergoing upper endoscopy, were lower among Asian and Afro‐Caribbean subjects compared with white individuals. There may also be a north–south gradient in the prevalence of gastro‐oesophageal reflux disease among western countries. Gastro‐oesophageal reflux disease may be moderately common in the Middle East. There are suggestions that the prevalence of gastro‐oesophageal reflux disease is increasing in the Far East.Conclusions : More data are required, especially from Africa, South America, the Middle East, and the Indian subcontinent. Suggestions are made regarding definitions and methodology to facilitate comparison between future studies from different countries.
Intestinal inflammation is a frequent feature of cystic fibrosis and is reduced by probiotic administration
Authors: Bruzzese E. , Raia V. , Gaudiello G. , Polito G. , Buccigrossi V. , Formicola V. , Guarino A. 
Published: September 2004

SummaryAims : To assess the incidence of intestinal inflammation in children with cystic fibrosis and to investigate whether probiotics decrease it.Study design : In this two‐phase, controlled, prospective study, faecal calprotectin was measured by enzyme‐linked immunosorbent assay in 30 children with cystic fibrosis, 30 healthy controls and 15 children with active inflammatory bowel disease. Ten children with cystic fibrosis received Lactobacillus GG, and faecal calprotectin was re‐measured 4 weeks later. Rectal nitric oxide production was measured with the rectal dialysis bag technique in 20 children with cystic fibrosis, 20 healthy controls and 15 children with inflammatory bowel disease. Five children with cystic fibrosis received Lactobacillus GG and nitric oxide was re‐measured 4 weeks later.Results : Mean faecal calprotectin was significantly higher in the two groups of patients than in controls. Abnormal values were detected in 27 of 30 cystic fibrosis and in 15 of 15 inflammatory bowel disease children. Also mean nitric oxide production was increased in both group of patients, and abnormal values were detected in 19 of 20 cystic fibrosis and in 15 of 15 inflammatory bowel disease children. Calprotectin and nitric oxide concentrations were reduced after probiotics administration.Conclusions : Intestinal inflammation is a major feature of cystic fibrosis and is reduced by probiotics. The latter finding suggests that intestinal microflora play a major role in intestinal inflammation in cystic fibrosis children.