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7. Experimental Infections with Leishmania Aethiopica and Immune Response Analysis of Cercopithecus Aethiops

Author

Menberework Chanyalew, Aseffa, Abraham, Harboe, Morten, Okao, Joseph Olobo, and Asrat Hailu

Subjects
parasitic diseases
Abstract

Background: Leishmania aethiopica (L. aethiopica) is the major cause of cutaneous leishmaniasis in Ethiopia. Only few studies are available on L. aethiopica infection in animal models. Therefore, the purpose of this study is to examine the possibility of establishing an African green monkey model and to describe the immunological consequences of L. aethiopica infection. Methods: Eight monkeys were inoculated subcutaneously at the tip of the nose with 5 x 106 L. aethiopica promastigotes. Six of them were inoculated with isolates from a patient with localized cutaneous leishmaniasis (LCL) and two were inoculated with isolates from a patient with diffused cutaneous leishmaniasis (DCL). Four control animals received only a sham inoculation of culture medium. Lymphocyte stimulation test was done and IFN-g levels were measured using a sandwich enzyme-linked immunosorbent assay (ELISA). Result: Three of the six monkeys infected with promastigotes from an LCL patient produced ulceration, one produced nodules that disappeared soon, and the other two lost hair at the infection site. One of the two monkeys infected with promastigotes from a DCL patient produced ulceration while the other lost hair at the infection site. The infection was further confirmed by the isolation of parasites from lesions of the animals. In the in vitro assay, Peripheral Blood Mononuclear Cell (PBMC) obtained from the infected and control animals showed comparable proliferative and IFN-g responses when stimulated with live or dead L. aethiopica parasites and soluble leishmanial antigen. Conclusion: The development of lesions suggests a possibility of using African green monkeys as a model to establish L. aethiopica infection. The lack of specificity in the proliferative response indicates the need to develop new specific antigens., Ethiopian Journal of Health and Biomedical Sciences, Vol. 2 No. 1 (2009): ETHIOPIAN JOURNAL OF HEALTH AND BIOMEDICAL SCIENCES

Published
2020
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11. COMMENTARY

Author

Harboe, Morten

Published
2007

12. The Role of Complement in Liver Injury, Regeneration, and Transplantation

Author

Thorgersen, Ebbe Billmann, Barratt-Due, Andreas, Haugaa, Hakon, Harboe, Morten, Pischke, Soren Erik, Nilsson, Per H., Mollnes, Tom Eirik, Thorgersen, Ebbe Billmann, Barratt-Due, Andreas, Haugaa, Hakon, Harboe, Morten, Pischke, Soren Erik, Nilsson, Per H., and Mollnes, Tom Eirik

Abstract

The liver is both an immunologically complex and a privileged organ. The innate immune system is a central player, in which the complement system emerges as a pivotal part of liver homeostasis, immune responses, and crosstalk with other effector systems in both innate and adaptive immunity. The liver produces the majority of the complement proteins and is the home of important immune cells such as Kupffer cells. Liver immune responses are delicately tuned between tolerance to many antigens flowing in from the alimentary tract, a tolerance that likely makes the liver less prone to rejection than other solid organ transplants, and reaction to local injury, systemic inflammation, and regeneration. Notably, complement is a double-edged sword as activation is detrimental by inducing inflammatory tissue damage in, for example, ischemia-reperfusion injury and transplant rejection yet is beneficial for liver tissue regeneration. Therapeutic complement inhibition is rapidly developing for routine clinical treatment of several diseases. In the liver, targeted inhibition of damaged tissue may be a rational and promising approach to avoid further tissue destruction and simultaneously preserve beneficial effects of complement in areas of proliferation. Here, we argue that complement is a key system to manipulate in the liver in several clinical settings, including liver injury and regeneration after major surgery and preservation of the organ during transplantation.

Published
2019
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14. The antigen 85 complex: a major secretion product of Mycobacterium tuberculosis

Author

Wiker, Harald G. and Harboe, Morten

Subjects
Mycobacterium tuberculosis -- Research, Antigens -- Analysis, Biological sciences
Abstract

Among the proteins secreted by the Mycobacterium tuberculosis and isolated for gene coding, the proteins of antigen 85 complex, labelled as 85A, 85B, and 85C, were found to be the most common. The 3 were encoded by 3 genes from various sites in the mycobacterium genome and shown to have extensive cross-reactivity and biochemical homology, though differing in molecular mass. The secreted mycobacterial antigens may be significant in the development of immunity and clinical symptoms.

Published
1992

16. Evidence for waning of latency in a cohort study of tuberculosis

Author

Bjune Gunnar A, Mustafa Tehmina, Wiker Harald G, and Harboe Morten

Subjects
Infectious and parasitic diseases, RC109-216
Abstract

Abstract Background To investigate how the risk of active tuberculosis disease is influenced by time since original infection and to determine whether the risk of reactivation of tuberculosis increases or decreases with age. Methods Cohort analysis of data for the separate ten year birth cohorts of 1876-1885 to 1959-1968 obtained from Statistics Norway and the National Tuberculosis Registry. These data were used to calculate the rates and the changes in the rates of bacillary (or active) tuberculosis. Data on bacillary tuberculosis for adult (20+) age groups were obtained from the National Tuberculosis Registry and Statistics Norway from 1946 to 1974. Most cases during this period arose due to reactivation of remote infection. Participants in this part of the analysis were all reported active tuberculosis cases in Norway from 1946 to 1974 as recorded in the National Tuberculosis Registry. Results Tuberculosis decreased at a relatively steady rate when following individual birth cohorts, but with a tendency of slower decline as time passed since infection. A mean estimate of this rate of decline was 57% in a 10 year period. Conclusions The risk of reactivation of latent tuberculosis decreases with age. This decline may reflect the rate at which latent tuberculosis is eliminated from a population with minimal transmission of tubercle bacilli. A model for risk of developing active tuberculosis as a function of time since infection shows that the rate at which tuberculosis can be eliminated from a society can be quite substantial if new infections are effectively prevented. The findings clearly indicate that preventative measures against transmission of tuberculosis will be the most effective. These results also suggest that the total population harbouring live tubercle bacilli and consequently the future projection for increased incidence of tuberculosis in the world is probably overestimated.

Published
2010
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22. Molecular modelling showed optimal fit between TSR5 in trimeric properdin and C345C in the C3b moiety for stabilization of the alternative convertase, whereas binding to molecular patterns in myeloperoxidase, endothelial cells and Neisseria meningitides was indirectly mediated by initial C3 activation

Author

Harboe, Morten, Johnson, Christina, Nymo, Stig, Ekholt, Karin, Schjalm, Camilla, Lindstad, Julie K., Pharo, Anne, Hellerud, Bernt C., Ekdahl, Kristina N., Mollnes, Tom E., Nilsson, Per H., Harboe, Morten, Johnson, Christina, Nymo, Stig, Ekholt, Karin, Schjalm, Camilla, Lindstad, Julie K., Pharo, Anne, Hellerud, Bernt C., Ekdahl, Kristina N., Mollnes, Tom E., and Nilsson, Per H.

Published
2016
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23. Molecular modelling showed optimal fit between TSR5 in trimeric properdin and C345C in the C3b moiety for stabilization of the alternative convertase, whereas binding to molecular patterns in myeloperoxidase, endothelial cells and Neisseria meningitides was indirectly mediated by initial C3 activation

Author

Harboe, Morten, primary, Johnson, Christina, additional, Nymo, Stig, additional, Ekholt, Karin, additional, Schjalm, Camilla, additional, Lindstad, Julie K., additional, Pharo, Anne, additional, Hellerud, Bernt C., additional, Ekdahl, Kristina N., additional, Mollnes, Tom E., additional, and Nilsson, Per H., additional

Published
2016
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28. The Role of Properdin in Zymosan- and Escherichia coli-Induced Complement Activation

Author

Harboe, Morten, Garred, Peter, Lindstad, Julie K, Pharo, Anne, Müller, Fredrik, Stahl, Gregory L, Lambris, John D, Mollnes, Tom Erik, Harboe, Morten, Garred, Peter, Lindstad, Julie K, Pharo, Anne, Müller, Fredrik, Stahl, Gregory L, Lambris, John D, and Mollnes, Tom Erik

Abstract

Properdin is well known as an enhancer of the alternative complement amplification loop when C3 is activated, whereas its role as a recognition molecule of exogenous pathogen-associated molecular patterns and initiator of complement activation is less understood. We therefore studied the role of properdin in activation of complement in normal human serum by zymosan and various Escherichia coli strains. In ELISA, microtiter plates coated with zymosan induced efficient complement activation with deposition of C4b and terminal complement complex on the solid phase. Virtually no deposition of C4b or terminal complement complex was observed with mannose-binding lectin (MBL)-deficient serum. Reconstitution with purified MBL showed distinct activation in both readouts. In ELISA, normal human serum-induced deposition of properdin by zymosan was abolished by the C3-inhibiting peptide compstatin. Flow cytometry was used to further explore whether properdin acts as an initial recognition molecule reacting directly with zymosan and three E. coli strains. Experiments reported by other authors were made with EGTA Mg(2+) buffer, permitting autoactivation of C3. We found inhibition by compstatin on these substrates, indicating that properdin deposition depended on initial C3b deposition followed by properdin in a second step. Properdin released from human polymorphonuclear cells stimulated with PMA did not bind to zymosan or E. coli, but when incubated in properdin-depleted serum this form of properdin bound efficiently to both substrates in a strictly C3-dependent manner, as the binding was abolished by compstatin. Collectively, these data indicate that properdin in serum as well as polymorphonuclear-released properdin is unable to bind and initiate direct alternative pathway activation on these substrates.

Published
2012

32. Critical Roles of Complement and Antibodies in Host Defense Mechanisms against Neisseria meningitidis as Revealed by Human Complement Genetic Deficiencies

Author

Hellerud, Bernt Christian, primary, Aase, Audun, additional, Herstad, Tove Karin, additional, Næss, Lisbeth Meyer, additional, Kristiansen, Lisa Høyem, additional, Trøseid, Anne-Marie Siebke, additional, Harboe, Morten, additional, Lappegård, Knut Tore, additional, Brandtzæg, Petter, additional, Høiby, E. Arne, additional, and Mollnes, Tom Eirik, additional

Published
2010
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46. Genetic complement deficiencies dissociate the roles of human complement in the inflammatory responses: Lessons from nature

Author

Lappegård, Knut Tore, primary, Christiansen, Dorte, additional, Pharo, Anne, additional, Thorgersen, Ebbe, additional, Hellerud, Bernt Christian, additional, Lindstad, Julie, additional, Nielsen, Erik, additional, Bergseth, Grethe, additional, Fadnes, Dag, additional, Abrahamsen, Tore, additional, Høiby, Arne, additional, Schejbel, Lone, additional, Garred, Peter, additional, Lambris, John D., additional, Harboe, Morten, additional, and Mollnes, Tom Eirik, additional

Published
2008
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47. Specificity of Subcapsular Antibody Responses in Ethiopian Patients following Disease Caused by Serogroup A Meningococci

Author

Norheim, Gunnstein, primary, Aseffa, Abraham, additional, Yassin, Mohammed Ahmed, additional, Mengistu, Getahun, additional, Kassu, Afework, additional, Fikremariam, Dereje, additional, Tamire, Wegene, additional, Merid, Yared, additional, Høiby, E. Arne, additional, Caugant, Dominique A., additional, Fritzsønn, Elisabeth, additional, Tangen, Torill, additional, Melak, Berhanu, additional, Berhanu, Degu, additional, Harboe, Morten, additional, Kolberg, Jan, additional, and Rosenqvist, Einar, additional

Published
2008
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49. Serum Antibody Responses in Ethiopian Meningitis Patients Infected with Neisseria meningitidis Serogroup A Sequence Type 7

Author

Norheim, Gunnstein, primary, Aseffa, Abraham, additional, Yassin, Mohammed Ahmed, additional, Mengistu, Getahun, additional, Kassu, Afework, additional, Fikremariam, Dereje, additional, Tamire, Wegene, additional, Merid, Yared, additional, Høiby, E. Arne, additional, Caugant, Dominique A., additional, Fritzsønn, Elisabeth, additional, Tangen, Torill, additional, Alebel, Tsegaye, additional, Berhanu, Degu, additional, Harboe, Morten, additional, and Rosenqvist, Einar, additional

Published
2007
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