Publications
111 results found
Dorr AD, Wilson MR, Wakabayashi K, et al., 2008, INJURIOUS VENTILATION AND INTRATRACHEAL LIPOPOLYSACCHARIDE INCREASE SOLUBLE TUMOUR NECROSIS FACTOR RECEPTORS IN THE ALVEOLI VIA TWO DISTINCT MECHANISMS, Winter Meeting of the British-Thoracic-Society, Publisher: B M J PUBLISHING GROUP, Pages: A71-A71, ISSN: 0040-6376
Scott AJ, Takata M, O'dea KP, 2008, REDOX MODIFICATION OF DITHIOLS/DISULPHIDES REGULATES TUMOUR NECROSIS FACTOR ALPHA-CONVERTING ENZYME ACTIVITY ON PRIMARY HUMAN MONOCYTES, Winter Meeting of the British-Thoracic-Society, Publisher: BMJ PUBLISHING GROUP, Pages: A141-A142, ISSN: 0040-6376
Dokpesi JO, O'Dea KP, Takata M, 2008, REGULATION OF MOUSE MONOCYTE TUMOUR NECROSIS FACTOR EXPRESSION BY PULMONARY ENDOTHELIAL CELLS IN VITRO, Winter Meeting of the British-Thoracic-Society, Publisher: B M J PUBLISHING GROUP, Pages: A72-A73, ISSN: 0040-6376
Vivas L, O'Dea KP, Noya O, et al., 2008, Hyperreactive malarial splenomegaly is associated with low levels of antibodies against red blood cell and <i>Plasmodium falciparum</i> derived glycolipids in Yanomami Amerindians from Venezuela, ACTA TROPICA, Vol: 105, Pages: 207-214, ISSN: 0001-706X
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- Citations: 3
O'Dea KP, Wilson MR, Dokpesi JO, et al., 2007, Lung-marginated monocytes play a central role in a two-hit LPS-zymosan model of acute lung injury in mice, Winter Meeting of the British-Thoracic-Society, Publisher: B M J PUBLISHING GROUP, Pages: A36-A37, ISSN: 0040-6376
Scott A, O'Dea KP, Smythe JF, et al., 2007, Lipopolysaccharide-induced upregulation of tumour necrosis factor-alpha converting enzyme activity on primary human monocytes, Winter Meeting of the British-Thoracic-Society, Publisher: B M J PUBLISHING GROUP, Pages: A114-A114, ISSN: 0040-6376
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- Citations: 2
Wilson MR, O'Dea KP, Zhang D, et al., 2007, Marginated monocytes exacerbate pulmonary oedema in a murine model of ventilator-induced lung injury, Winter Meeting of the British-Thoracic-Society, Publisher: B M J PUBLISHING GROUP, Pages: A61-A62, ISSN: 0040-6376
Wilson MR, Goddard ME, O'Dea KP, et al., 2007, Differential roles of p55 and p75 tumor necrosis factor receptors on stretch-induced pulmonary edema in mice, AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY, Vol: 293, Pages: L60-L68, ISSN: 1040-0605
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- Citations: 58
Shearman AD, Wilson MR, O'Dea KP, et al., 2007, High stretch mechanical ventilation promotes the recruitment of activated inflammatory subset monocytes to the lung in mice, Meeting of the Anaesthetic-Research-Society, Publisher: OXFORD UNIV PRESS, Pages: 289P-290P, ISSN: 0007-0912
Blackbeard J, O'Dea K, Wallace VCJ, et al., 2007, Quantification of the rat spinal microglial response to peripheral nerve injury as revealed by immunohistochemical image analysis and flow cytometry., J.Neurosci.Methods, Vol: 164, Pages: 207-217
Alvarez-Iglesias M, Wayne G, O'Dea KP, et al., 2005, Continuous real-time measurement of tumor necrosis factor-alpha converting enzyme activity on live cells.
O'Dea KP, Young AJ, Yamamoto H, et al., 2005, Lung-marginated monocytes modulate pulmonary microvascular injury during early endotoxemia.
Choudhury S, Wilson MR, Goddard ME, et al., 2004, Mechanisms of early pulmonary neutrophil sequestration in ventilator-induced lung injury in mice, AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY, Vol: 287, Pages: L902-L910, ISSN: 1040-0605
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- Citations: 79
Choudhury S, Wilson MR, Goddard ME, et al., 2004, Mechanisms of early pulmonary neutrophil sequestration in ventilator-induced lung injury in mice., Pages: 902-910
Wilson MR, Choudhury S, Goddard ME, et al., 2003, High tidal volume upregulates intrapulmonary cytokines in an in vivo mouse model of ventilator-induced lung injury, JOURNAL OF APPLIED PHYSIOLOGY, Vol: 95, Pages: 1385-1393, ISSN: 8750-7587
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- Citations: 166
O'Dea KP, Pasvol G, 2003, Optimal tumor necrosis factor induction by <i>Plasmodium falciparum</i> requires the highly localized release of parasite products, INFECTION AND IMMUNITY, Vol: 71, Pages: 3155-3164, ISSN: 0019-9567
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- Citations: 8
O'Dea KP, McKean PG, Brown KN, 2002, <i>Plasmodium chabaudi chabaudi</i> AS:: modification of acute infection in CBA/Ca mice as a result of pre-treatment with erythrocyte band 3 in adjuvant, EXPERIMENTAL PARASITOLOGY, Vol: 102, Pages: 66-71, ISSN: 0014-4894
O'Dea KP, McKean PG, Jarra W, et al., 1996, A single gene copy merozoite surface antigen and immune evasion?, Parasite Immunol, Vol: 18, Pages: 165-172, ISSN: 0141-9838
During the course of chronic malaria infection antigenic variants of a parasite antigen are expressed and exposed on the surface of infected erythrocyte membranes. There also exists a number of apparently invariant single gene copy blood-stage antigens, exposed or non-exposed, which have been shown to afford immunity under experimental conditions. To determine why the host, presented with invariant 'protective' antigens, is unable to control infections effectively, immunity to a representative single gene copy antigen, the merozoite surface protein 1 (MSP1) was investigated in Plasmodium chabaudi chabaudi AS, a murine model of chronic malaria. Immunization with monoclonal antibody affinity purified native MSP1 resulted in enhanced control of parasitaemia on challenge, irrespective of the parasite inoculum size; challenge with a single parasite, however, suggested that expansion of resistant parasite subpopulations was not occurring. Challenge of mice immunized with recombinant fusion proteins encoding N- or C-terminal regions of the P.c. chabaudi AS MSP1 produced inconsistent effects, often parasitaemias were indistinguishable from controls despite significant anti-MSP1 antibody responses. The not unlikely contamination of MSP1 native preparations with erythrocyte (E) components was considered. Immunization with a mixture of the MSP1 C-terminus recombinant polypeptide and a Triton X-100 solubilized lysate of normal E resulted in enhanced control of parasitaemia, however, no effect was seen after administration of either component on its own. Co-immunization of E with the N-terminus polypeptide reversed the inhibition seen, on this occasion with this construct alone.
O'Dea KP, McKean PG, Harris A, et al., 1995, Processing of the Plasmodium chabaudi chabaudi AS merozoite surface protein 1 in vivo and in vitro., Mol Biochem Parasitol, Vol: 72, Pages: 111-119, ISSN: 0166-6851
Processing of the Plasmodium merozoite surface protein 1 (MSP-1) has been described for parasites maintained under in vitro conditions. We have now demonstrated, using CBA/Ca mice infected with Plasmodium chabaudi chabaudi AS, that MSP-1 processing also occurs in vivo. The major proteolytic cleavage sites and a processing scheme were deduced from N-terminal amino-acid sequences of the MSP-1 breakdown products. Comparison of MSP-1 processing in P. falciparum and P.c. chabaudi indicates a degree of conservation and in two cases the position of protease cleavage appears identical. Significant amounts of MSP-1 polypeptides are found in plasma during schizogony. Various aspects of MSP-1 processing including immunological and physiological reactions in the host during the critical period of schizogony can now be examined in vivo.
McKean PG, O'Dea K, Brown KN, 1993, Nucleotide sequence analysis and epitope mapping of the merozoite surface protein 1 from Plasmodium chabaudi chabaudi AS., Mol Biochem Parasitol, Vol: 62, Pages: 199-209, ISSN: 0166-6851
The complete nucleotide sequence of the gene encoding the merozoite surface protein 1 (MSP-1) from the rodent malaria parasite Plasmodium chabaudi chabaudi AS has been determined by direct sequencing of overlapping PCR derived fragments. Comparison of the P. c. chabaudi AS nucleotide sequence with the previously published P. c. chabaudi IP-PC1 sequence indicates that although the MSP-1 gene of these two P. c. chabaudi strains is highly conserved, with sequence identity often approaching 100%, interspersed throughout the molecule are 5 regions of divergence. This is at variance with published data which suggested that the P. c. chabaudi AS and P. c. chabaudi IP-PC1 MSP-1 sequences are largely identical. Epitope mapping studies with a panel of anti-P. c. chabaudi AS MSP-1 monoclonal antibodies demonstrate that whilst most of these mAbs recognise epitopes at the N-terminus of the MSP-1 molecule, two mAbs, including one capable of inhibiting challenge infections in mice in an in vivo passive transfer assay, recognise epitopes which map to the C-terminus.
McKean PG, O'Dea K, Brown KN, 1993, A single amino acid determines the specificity of a monoclonal antibody which inhibits Plasmodium chabaudi AS in vivo., Mol Biochem Parasitol, Vol: 62, Pages: 211-221, ISSN: 0166-6851
The in vivo inhibitory action of NIMP23, a monoclonal antibody raised against the rodent parasite Plasmodium chabaudi chabaudi AS, has previously been shown to be strain-specific, capable of delaying significantly the onset of P. c. chabaudi AS but not a P. c. chabaudi CB challenge parasitaemia. The epitope to which this mAb binds has been mapped to the second of two epidermal growth factor-like domains located at the C-terminus of the merozoite surface protein 1 (MSP-1) of P. c. chabaudi AS. The C-terminus region of the MSP-1 of P. c. chabaudi is a region of heterogeneity with AS and CB strain parasites showing only 78% identity at the amino acid level. The critical amino acid substitution which accounts for the strain specificity of the NIMP23 monoclonal antibody has now been identified. Polymerase chain reaction directed mutagenesis experiments demonstrate that a single proline to asparagine substitution at position 1722 in the primary amino acid sequence is sufficient to convert NIMP23-negative P. c. chabaudi CB expression constructs into NIMP23-positive clones whilst the converse substitution of an asparagine for a proline residue converts P. c. chabaudi AS expression constructs into NIMP23-negative clones.
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