Microbiology and Immunology publications
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Item Metadata only TGT-β and endothelial cells inhibit VCAM-1 expression on human vascular smooth muscle cells(American Heart Association, 1995) Gamble, Jennifer R.; Bradley, Sandy; Noack, Leanne; Vadas, Mathew AlexanderVascular smooth muscle cells (VSMCs) are normally devoid of the adhesion protein vascular cell adhesion molecule–1 (VCAM-1), which has, however, been observed on human VSMCs in atheroma. We now show that cultured human saphenous vein VSMCs express small amounts of VCAM-1 and that the cytokine tumor necrosis factor–α (TNF-α) induces, in a time- and dose-dependent fashion, a significant increase in its expression. Interleukin (IL)-4, IL-1, and to a lesser extent interferon gamma have similar effects. TNF-α–stimulated human VSMCs demonstrate increased binding of T lymphocytes that is totally VCAM-1 mediated. The cytokine transforming growth factor–β (TGF-β) at 2.0 ng/mL inhibited basal VCAM-1 expression by 84±8% and the induction by TNF-α by between 56±16% and 77±15% depending on the dose of TNF. Furthermore, coculture on opposing sides of a polycarbonate filter of human VSMCs with human umbilical vein endothelial cells also inhibited the induction of VCAM-1 by 47±6%. As active TGF-β is produced upon the coculture of VSMCs and endothelial cells, we suggest that the close physical proximity of these cells in vivo is responsible for the lack of expression of VCAM-1 on VSMCs and that the interruption of this contact in atheroma is an important pathogenic event. As VCAM-1 not only serves as an adhesion molecule but also as a costimulator of immune cells, its expression may be crucial in the propagation of vascular lesions.Item Metadata only Role of cytokines in endothelial cell functions(Blackwell Science, 1995) Litwin, M. S.; Gamble, Jennifer R.; Vadas, Mathew Alexander; School of Molecular and Biomedical Science : Microbiology and ImmunologyItem Metadata only High density lipoproteins inhibit cytokine-induced expression of endothelial cell adhesion molecules.(American Heart Association, 1995) Cockerill, Gillian W.; Rye, Kerry-Anne; Gamble, Jennifer R.; Vadas, Mathew Alexander; Barter, Philip JohnWhile an elevated plasma concentration of HDLs is protective against the development of atherosclerosis and ensuing coronary heart disease (CHD), the mechanism of this protection is unknown. One early cellular event in atherogenesis is the adhesion of mononuclear leukocytes to the endothelium. This event is mediated principally by vascular cell adhesion molecule-1 (VCAM-1) but also involves other molecules, such as intercellular adhesion molecule-1 (ICAM-1) and E-selectin. We have investigated the effect of isolated plasma HDLs and reconstituted HDLs on the expression of these molecules by endothelial cells. We show that physiological concentrations of HDLs inhibit tumor necrosis factor-α (TNF-α) or interleukin-1 (IL-1) induction of these leukocyte adhesion molecules in a concentration-dependent manner. Steady state mRNA levels of TNF-α–induced VCAM-1 and E-selectin are significantly reduced by physiological concentrations of HDLs. At an HDL concentration of 1 mg/mL apolipoprotein A-I, the protein expressions of VCAM-1, ICAM-1, and E-selectin were inhibited by 89.6±0.4% (mean±SD, n=4), 64.8±1.0%, and 79.2±0.4%, respectively. In contrast, HDLs have no effect on the expression of platelet endothelial cell adhesion molecule (PECAM) or on the expression of the p55 and p75 subunits of the TNF-α receptor. HDLs were effective when added from 16 hours before to 5 minutes after cytokine stimulation. HDLs had no effect on TNF-α–induced expression of ICAM-1 by human foreskin fibroblasts, suggesting that the effect is cell-type restricted. This study provides the first evidence that HDLs may protect against CHD by inhibiting the expression of adhesion molecules, which are required for the interaction between leukocytes and the endothelium.Item Metadata only Stepwise analysis of reverse transcription in a cell-to-cell HIV infection model: kinetics and implications(Society for General Microbiology, 1995) Karageorgos, L.; Li, P.; Burrell, C.Item Metadata only A beginning to cell surface studies in Vibrio cholerae: a personal perspective(Institut Pasteur / Elsevier, 1995) Manning, Paul AlexanderItem Metadata only Terbinafine in onychomycosis(C. V. Mosby, 1995) Watson, A.; Marley, J.; Ellis, D.; Williams, T.Item Metadata only Thymine auxotrophy as an attenuating marker in Vibrio cholerae(Academic Press Limited, 1995) Attridge, Stephen RichardItem Metadata only Regulation of granulocyte-macrophage colony-stimulating factor and E-selection expression in endothelial cells by cyclosporin A and the T cell transcription factor NFAT.(Grune and Stratton, 1995) Cockerill, G. W.; Bert, Andrew G.; Ryan, Gregory Robert; Gamble, Jennifer R.; Vadas, Mathew Alexander; Cockerill, Peter N.Item Metadata only Transendothelial migration of neutrophils involves integrin-associated protein (DC47)(National Academy of Sciences of the United States of America, 1995) Cooper, D. Lindberg; Gamble, Jennifer R.; Brown, E. J.; Vadas, Mathew AlexanderItem Metadata only Comparative toxicity and virulence of Escherichia coli clones expressing variant and chimeric Shiga-like toxin type II operons(American Society for Microbiology, 1995) Paton, A.; Bourne, A.; Manning, P.; Paton, J.Shiga-like toxin (SLT)-producing strains of Escherichia coli are known to cause diarrhea, hemorrhagic colitis, and hemolytic-uremic syndrome in humans. The SLTs, particularly those related to type II (SLT-II), are a diverse family of toxins which may have differing in vitro or in vivo properties. To examine the impact of naturally occurring SLT-II sequence variation on the capacity of a given E. coli strain to cause disease, operons encoding four different SLT-II-related toxins, designated SLT-II/O111, SLT-II/OX3a, SLT-II/OX3b, and SLTII/ O48, were cloned in the same orientation in pBluescript. French pressure cell lysates of E. coli DH5a derivatives carrying these plasmids differed markedly in cytotoxicity for Vero cells, with 50% cytotoxic doses ranging from 20 to 328,000/ml. The strains also differed in oral virulence for streptomycin-treated mice, as judged by survival rate and/or median survival time, but virulence did not necessarily correlate with in vitro cytotoxicity. The SLT-II type associated with the lowest oral virulence was SLT-II/O111. Both the overall survival rate and the median survival time of mice challenged with clones producing this toxin were significantly greater than that for mice challenged with a clone producing the closely related SLT-II/OX3a. Experiments with clones carrying chimeric O111/OX3a SLT-II operons indicated that the reduced virulence was associated with an Arg-1763Gly substitution in the mature A subunit. Clones producing SLT-II/O48 and SLT-II/OX3b had similarly high cytotoxicities for Vero cells, but the latter was more virulent when fed to streptomycin-treated mice, as judged by median survival time. Experiments with clones carrying chimeric O48/OX3b SLT-II operons indicated that the increased virulence was a function of the A subunit of SLT-II/ OX3b, which differs from the A subunit of SLT-II/O48 by only two amino acids (Met-43Thr and Gly-1023Asp, respectively). These findings raise the possibility that naturally occurring SLT-II sequence variations may impact directly on the capacity of a given SLT-producing E. coli strain to cause disease.Item Metadata only Interferon g upregulates IL-3 receptor expression in human endothelial cells and synergises with IL-3 in stimulating MHC class II expression and cytokine production(Grune and Stratton, 1995) Korpelainen, Eija; Gamble, Jennifer R.; Smith, William B.; Dottore, Mara; Vadas, Mathew AlexanderItem Metadata only Relationships withing the Rugopharynx delta species complex (Nematoda: Strongyloidea) from Australian marsupials inferred from allozyme electrophoresis(Kluwer Academic Publishers, 1995) Beveridge, Ian; Chilton, Neil B.; Andrews, Ross HectorRelationships between the strongyloid nematodesRugopharynx delta, R. zeta, R. omega, R. longibursaris, R. mawsonae andR. sigma, all from macropodid marsupials, were investigated using allozyme data. The phylogenetic trees derived from the electrophoretic data set were congruent with those of the hosts and were consistent with the hypothesis that the species complex originated in pademelons of the genusThylogale and diversified in rock-wallabies (Petrogale spp.) and scrub wallabies of the subgenusNotamacropus. Host switching is evident only between closely related macropodid taxa.Item Metadata only Cytokines increase human haemopoietic cell adhesiveness by activation of very late antigen (VLA)-4 and VLA-5 integrins(Rockefeller Institute for Medical Research, 1995) Levesque, Jean-Pierre; Leavesley, David I.; Niutta, Silvana; Vadas, Mathew Alexander; Simmons, Paul J.Item Metadata only Use of confocal microscopy in studying bacterial adherence and invasion. Methods in enyzmology(Academic Press, 1995) Manning, Paul Alexander; School of Molecular and Biomedical Science : Microbiology and ImmunologyItem Metadata only Neutrophils activated by granulocyte-macrophage colony-stimulating factor express receptors for interleukin-3 which mediate class II expression(American Society of Hematology, 1995) Smith, W.; Guida, L.; Qiuy, S.; Korpelainen, E.; van den Hueven, C.; Gillis, D.; Hawrylowicz, C.; Vadas, M.; Lopez, A.Freshly isolated peripheral blood neutrophils, unlike monocytes and eosinophils, do not bind interleukin-3 (IL-3) or respond to IL-3). We show that neutrophils cultured for 24 hours in granulocyte-macrophage colony-stimulating factor (GM-CSF) express mRNA for the IL-3 receptor (R) alpha subunit, as shown by RNase protection assays, and IL-3R alpha chain protein, as shown by cytometric analysis using two different specific monoclonal antibodies. This effect was selective for GM-CSF, because granulocyte colony-stimulating factor, tumor necrosis factor- alpha, interferon-gamma, and IL-1 failed to induce the IL-3 receptor. Saturation binding curves with 125I-IL-3 and Scatchard transformation showed the presence of about 100 high-affinity and 4,000 low-affinity receptors. Because neutrophils have been shown to express human leukocyte antigen (HLA)-DR in response to GM-CSF, we examined the possibility that IL-3 could augment HLA-DR expression on GM-CSF-treated cells. We found that neutrophils incubated with 30 ng/mL IL-3 as well as 0.1 ng/mL GM-CSF expressed a mean of 2.1-fold higher levels of HLA- DR than with GM-CSF alone (P < .005), confirming the signaling competence of the newly expressed IL-3R. This increase was seen even at maximal concentrations of GM-CSF and IL-3 can have an additive effect on mature human cells. The augmentation of HLA-DR by IL-3 was specific because it could be inhibited by a blocking anti-IL-3R antibody. Expression of class II molecules by neutrophils under these conditions may have significance for antigen presentation. These results provide further evidence for the role of GM-CSF as an amplification factor in inflammation by inducing neutrophil responsiveness to IL-3 produced by T cells or mast cells.Item Metadata only In Vibrio cholerae O1 rfaD is linked closely to rfb operon(Elsevier, 1995) Stroeher, U.; Karageorgos, L.; Morona, R.; Manning, P.Item Metadata only Strongyloides stercoralis: A conundrum for gastroenterologists(B.M.J. Publishing Group, 1995) Grove, D. I.; School of Molecular and Biomedical Science : Microbiology and ImmunologyItem Metadata only Transcriptional regulation of mouse granulocyte-macrophage colony-stimulating factor/IL-3 locus(Williams & Wilkins Co., 1995) Osborne, Cameron Stuart; Vadas, Mathew Alexander; Cockerill, Peter N.Item Metadata only Lack of evidence for hepatitis B transmission in Australian Rules footballers(Australasian Medical Publishing Co., 1995) Siebert, D.; Burrell, C.Objective
To determine the prevalence of markers of past hepatitis B infection among participants in Australian Rules football, to estimate the potential exposure of Australians to hepatitis B virus (HBV) in contact sport.Design and setting
A point prevalence survey for antibody to hepatitis B surface antigen (anti-HBs) and core antigen (anti-HBc), supported by a questionnaire used to determine the history of risk and exposure, in South Australian National Football League (SANFL) players supervised at club level by general practitioners and sports medicine specialists.Participants
Of 245 players from seven clubs, 49 were excluded from the study because they had been previously vaccinated. Of 196 eligible participants, 117 submitted blood samples and, of these, 85 returned questionnaires.Results
One player was positive for anti-HBc (a prevalence rate of 0.85%). This individual and three anti-HBc-negative players were positive for anti-HBs in the absence of a history of vaccination. We could not ascertain whether these additional three players had been previously infected, or vaccinated without this fact having been recorded on the questionnaires. No single behavioural factor correlated with positive anti-HBs results.Conclusions
The prevalence of markers of past hepatitis B infection in SANFL football players was no different to that in blood donors of the same age group from the same city. There was no evidence for any additional HBV transmission due to participation in football over that in the blood donor population. Vaccination of footballers and people engaged in similar sports is of benefit in conferring protection on the individual, but would be unlikely to make a significant public health impact on community rates of HBV infection.Item Metadata only Regulation of tcpgenes in classical and El Tor strains of Vibrio cholerae O1(Elsevier, 1995) Thomas, Sonia; Williams, Susan G.; Manning, Paul Alexander; Department of Microbiology and ImmunologyExpression of genes encoding the toxin-co-regulated pilus (TCP) varies between the two biotypes of Vibrio cholerae O1. Sequence analysis of the tcp locus from the classical and El Tor strains has revealed differences in the intergenic regions between tcpI and tcpP, and tcpH and tcpA, which may be involved in regulation. To investigate this possibility, transcription of tcpA, and the predicted upstream promoters for tcpI and tcpP, has been analysed in the classical and El Tor strains using promoter-cat (chloramphenicol acetyltransferase) fusions. Together with primer extension analyses, these studies indicate that the tcpA and tcpP promoters are toxR-dependent and suggest that TcpP may be involved in activation of both the tcpI and tcpP promoters. We conclude that differences in the level of tcpA expression in a classical and an El Tor strain are likely to be due to the effect of sequence variation on the ability of control factors to act on these regulatory regions.