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5 results on '"Dallman, Maggie J."'

1. Integrated cytokine and metabolic analysis of pathological\ud responses to parasite exposure in rodents

Author

Saric, Jasmina, Li, Jia V., Swann, Jonathan, Utzinger, Jurg, Calvert, Gail, Nicholson, Jeremy K., Dirnhofer, Stephan, Dallman, Maggie J., Bictash, Magda, and Holmes, Elaine

Subjects
parasitic diseases
Abstract

Parasitic infections cause a myriad of responses in their mammalian hosts, on immune as well as on metabolic level. A multiplex panel of cytokines and metabolites derived from four parasite-rodent models, namely, Plasmodium berghei-mouse, Trypanosoma brucei brucei-mouse, Schistosoma mansoni-mouse, and Fasciola hepatica-rat were statistically coanalyzed. 1H NMR spectroscopy and multivariate statistical analysis were used to characterize the urine and plasma metabolite profiles in infected and noninfected animals. Each parasite generated a unique metabolic signature in the host. Plasma cytokine concentrations were obtained using the ‘Meso Scale Discovery’ multi cytokine assay platform. Multivariate data integration methods were subsequently used to elucidate the component of the metabolic signature which is associated with inflammation and to determine specific metabolic correlates with parasite-induced changes in plasma cytokine levels. For example, the relative levels of acetyl glycoproteins extracted from the plasma metabolite profile in the P. berghei-infected mice were statistically correlated with IFN-γ, whereas the same cytokine was anticorrelated with glucose levels. Both the metabolic and the cytokine data showed a similar spatial distribution in principal component analysis scores plots constructed for the combined murine data, with samples from all infected animals clustering according to the parasite species and whereby the protozoan infections (P. berghei and T. b. brucei) grouped separately from the helminth infection (S. mansoni). For S. mansoni, the main infection-responsive cytokines were IL-4 and IL-5, which covaried with lactate, choline, and D-3-hydroxybutyrate. This study demonstrates that the inherently differential immune response to single and multicellular parasites not only manifests in the cytokine expression, but also consequently imprints on the metabolic signature, and calls for in-depth analysis to further explore direct links between immune features and biochemical pathways.

Published
2010

4. Human neural graft function in rats treated with antiinterleukin II receptor antibody

Author

Honey, Christopher R., Clarke, Debbie J., Dallman, Maggie J., and Charlton, Harry M.

Abstract

PROLONGED immunosuppression with cyclosporin A allows survival of human xenografts in the rat Parkinsonian model but the drug has side effects. Ideally immunosuppression should be of short duration, to minimize the chance of infection, yet be capable of supporting long term survival of the transplanted tissue. We report that short term treatment with an anti-rat interleukin II receptor (IL2R) monoclonal antibody (MAb) resulted in apparently permanent survival of human fetal dopaminergic grafts in “Parkinsonian” rats. The recipients remained healthy and the excellent survival of the transplants suggests that the antibody injection strategy would almost certainly abrogate allograft rejection and raises the possibility that xenogenic dopaminergic neurones could be used as donor tissue in humans.

Published
1990

5. Integrated cytokine and metabolic analysis of pathological responses to parasite exposure in rodents.

Author

Saric J, Li JV, Swann JR, Utzinger J, Calvert G, Nicholson JK, Dirnhofer S, Dallman MJ, Bictash M, and Holmes E

Subjects
Animals, Discriminant Analysis, Disease Models, Animal, Fasciola hepatica physiology, Female, Histocytochemistry, Mice, Multivariate Analysis, Nuclear Magnetic Resonance, Biomolecular, Parasitic Diseases blood, Parasitic Diseases pathology, Phenotype, Plasmodium berghei physiology, Principal Component Analysis, Rats, Schistosoma mansoni physiology, Trypanosoma brucei brucei physiology, Cytokines metabolism, Host-Parasite Interactions, Metabolome, Parasitic Diseases metabolism, Parasitic Diseases parasitology
Abstract

Parasitic infections cause a myriad of responses in their mammalian hosts, on immune as well as on metabolic level. A multiplex panel of cytokines and metabolites derived from four parasite-rodent models, namely, Plasmodium berghei-mouse, Trypanosoma brucei brucei-mouse, Schistosoma mansoni-mouse, and Fasciola hepatica-rat were statistically coanalyzed. (1)H NMR spectroscopy and multivariate statistical analysis were used to characterize the urine and plasma metabolite profiles in infected and noninfected animals. Each parasite generated a unique metabolic signature in the host. Plasma cytokine concentrations were obtained using the 'Meso Scale Discovery' multi cytokine assay platform. Multivariate data integration methods were subsequently used to elucidate the component of the metabolic signature which is associated with inflammation and to determine specific metabolic correlates with parasite-induced changes in plasma cytokine levels. For example, the relative levels of acetyl glycoproteins extracted from the plasma metabolite profile in the P. berghei-infected mice were statistically correlated with IFN-gamma, whereas the same cytokine was anticorrelated with glucose levels. Both the metabolic and the cytokine data showed a similar spatial distribution in principal component analysis scores plots constructed for the combined murine data, with samples from all infected animals clustering according to the parasite species and whereby the protozoan infections (P. berghei and T. b. brucei) grouped separately from the helminth infection (S. mansoni). For S. mansoni, the main infection-responsive cytokines were IL-4 and IL-5, which covaried with lactate, choline, and d-3-hydroxybutyrate. This study demonstrates that the inherently differential immune response to single- and multicellular parasites not only manifests in the cytokine expression, but also consequently imprints on the metabolic signature, and calls for in-depth analysis to further explore direct links between immune features and biochemical pathways.

Published
2010
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