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1. Structure-function analysis of time-resolved immunological phases in metabolic dysfunction-associated fatty liver disease (MASH) comparing the NIF mouse model to human MASH

Author

Schmidt-Christensen, Anja, Eriksson, Gustaw, Laprade, William M., Pirzamanbein, Behnaz, Hörnberg, Maria, Linde, Kajsa, Nilsson, Julia, Skarsfeldt, Mark, Leeming, Diana J., Mokso, Rajmund, Verezhak, Mariana, Dahl, Anders, Dahl, Vedrana, Önnerhag, Kristina, Oghazi, Massoud Rezaee, Mayans, Sofia, and Holmberg, Dan

Published
2024
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8. A Plasmodium cysteine protease required for efficient transition from the liver infection stage

Author

Putrianti, Elyzana Dewi, Schmidt-Christensen, Anja, Heussler, Volker, Matuschewski, Kai, and Ingmundson, Alyssa

Subjects
Plasmodium berghei, QH301-705.5, Protozoan Proteins, 570 Biologie, RC581-607, Malaria, Rats, Rats, Sprague-Dawley, Mice, Liver, Cysteine Proteases, ddc:570, parasitic diseases, Animals, 570 Life sciences, biology, Immunologic diseases. Allergy, Biology (General)
Abstract

The transitions between developmental stages are critical points in the Plasmodium life cycle. The development of Plasmodium in the livers of their mammalian hosts bridges malaria transmission and the onset of clinical symptoms elicited by red blood cell infection. The egress of Plasmodium parasites from the liver must be a carefully orchestrated process to ensure a successful switch to the blood stage of infection. Cysteine protease activity is known to be required for liver-stage Plasmodium egress, but the crucial cysteine protease(s) remained unidentified. Here, we characterize a member of the papain-like cysteine protease family, Plasmodium berghei serine repeat antigen 4 (PbSERA4), that is required for efficient initiation of blood-stage infection. Through the generation PbSERA4-specific antisera and the creation of transgenic parasites expressing fluorescently tagged protein, we show that PbSERA4 is expressed and proteolytically processed in the liver and blood stages of infection. Targeted disruption of PbSERA4 results in viable and virulent blood-stage parasites. However, upon transmission from mosquitoes to mice, Pbsera4(-) parasites displayed a reduced capacity to initiate a new round of asexual blood-stage replication. Our results from cultured cells indicate that this defect results from an inability of the PbSERA4-deficient parasites to egress efficiently from infected cells at the culmination of liver-stage development. Protection against infection with wildtype P. berghei could be generated in animals in which Pbsera4(-) parasites failed to establish infection. Our findings confirm that liver-stage merozoite release is an active process and demonstrate that this parasite-encoded cysteine protease contributes to parasite escape from the liver.

Published
2020
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12. Optical projection tomography for rapid whole mouse brain imaging

Author

Nguyen, David, primary, Marchand, Paul J., additional, Planchette, Arielle L., additional, Nilsson, Julia, additional, Sison, Miguel, additional, Extermann, Jérôme, additional, Lopez, Antonio, additional, Sylwestrzak, Marcin, additional, Sordet-Dessimoz, Jessica, additional, Schmidt-Christensen, Anja, additional, Holmberg, Dan, additional, Van De Ville, Dimitri, additional, and Lasser, Theo, additional

Published
2017
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13. A New Mouse Model That Spontaneously Develops Chronic Liver Inflammation and Fibrosis

Author

Fransen-Pettersson, Nina, Duarte, Nadia, Nilsson, Julia, Lundholm, Marie, Mayans, Sofia, Larefalk, Åsa, Hannibal, Tine D., Hansen, Lisbeth, Schmidt-Christensen, Anja, Ivars, Fredrik, Cardell, Susanna, Palmqvist, Richard, Rozell, Bjoern, Holmberg, Dan, Fransen-Pettersson, Nina, Duarte, Nadia, Nilsson, Julia, Lundholm, Marie, Mayans, Sofia, Larefalk, Åsa, Hannibal, Tine D., Hansen, Lisbeth, Schmidt-Christensen, Anja, Ivars, Fredrik, Cardell, Susanna, Palmqvist, Richard, Rozell, Bjoern, and Holmberg, Dan

Abstract

Here we characterize a new animal model that spontaneously develops chronic inflammation and fibrosis in multiple organs, the non-obese diabetic inflammation and fibrosis (N-IF) mouse. In the liver, the N-IF mouse displays inflammation and fibrosis particularly evident around portal tracts and central veins and accompanied with evidence of abnormal intrahepatic bile ducts. The extensive cellular infiltration consists mainly of macrophages, granulocytes, particularly eosinophils, and mast cells. This inflammatory syndrome is mediated by a transgenic population of natural killer T cells (NKT) induced in an immunodeficient NOD genetic background. The disease is transferrable to immunodeficient recipients, while polyclonal T cells from unaffected syngeneic donors can inhibit the disease phenotype. Because of the fibrotic component, early on-set, spontaneous nature and reproducibility, this novel mouse model provides a unique tool to gain further insight into the underlying mechanisms mediating transformation of chronic inflammation into fibrosis and to evaluate intervention protocols for treating conditions of fibrotic disorders.

Published
2016
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15. A New Mouse Model That Spontaneously Develops Chronic Liver Inflammation and Fibrosis

Author

Fransén-Pettersson, Nina, primary, Duarte, Nadia, additional, Nilsson, Julia, additional, Lundholm, Marie, additional, Mayans, Sofia, additional, Larefalk, Åsa, additional, Hannibal, Tine D., additional, Hansen, Lisbeth, additional, Schmidt-Christensen, Anja, additional, Ivars, Fredrik, additional, Cardell, Susanna, additional, Palmqvist, Richard, additional, Rozell, Björn, additional, and Holmberg, Dan, additional

Published
2016
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16. E2-2 Dependent Plasmacytoid Dendritic Cells Control Autoimmune Diabetes

Author

Hansen, Lisbeth, Schmidt-Christensen, Anja, Gupta, Shashank, Fransen-Pettersson, Nina, Hannibal, Tine D., Reizis, Boris, Santamaria, Pere, Holmberg, Dan, Hansen, Lisbeth, Schmidt-Christensen, Anja, Gupta, Shashank, Fransen-Pettersson, Nina, Hannibal, Tine D., Reizis, Boris, Santamaria, Pere, and Holmberg, Dan

Published
2015

18. Longitudinal three-dimensional visualisation of autoimmune diabetes by functional optical coherence imaging

Author

Berclaz, Corinne, primary, Schmidt-Christensen, Anja, additional, Szlag, Daniel, additional, Extermann, Jerome, additional, Hansen, Lisbeth, additional, Bouwens, Arno, additional, Villiger, Martin, additional, Goulley, Joan, additional, Schuit, Frans, additional, Grapin-Botton, Anne, additional, Lasser, Theo, additional, and Holmberg, Dan, additional

Published
2015
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19. The Plasmodium serine-type SERA proteases display distinct expression patterns and non-essential in vivo roles during life cycle progression of the malaria parasite

Author

Heussler, Volker, Schmidt-Christensen, Anja, Matuschewski, Kai, Arnold, Iris, Silvie, Olivier, and Putrianti, Elyzana D

Subjects
570 Life sciences, biology
Abstract

Parasite proteases play key roles in several fundamental steps of the Plasmodium life cycle, including haemoglobin degradation, host cell invasion and parasite egress. Plasmodium exit from infected host cells appears to be mediated by a class of papain-like cysteine proteases called 'serine repeat antigens' (SERAs). A SERA subfamily, represented by Plasmodium falciparum SERA5, contains an atypical active site serine residue instead of a catalytic cysteine. Members of this SERAser subfamily are abundantly expressed in asexual blood stages, rendering them attractive drug and vaccine targets. In this study, we show by antibody localization and in vivo fluorescent tagging with the red fluorescent protein mCherry that the two P. berghei serine-type family members, PbSERA1 and PbSERA2, display differential expression towards the final stages of merozoite formation. Via targeted gene replacement, we generated single and double gene knockouts of the P. berghei SERAser genes. These loss-of-function lines progressed normally through the parasite life cycle, suggesting a specialized, non-vital role for serine-type SERAs in vivo. Parasites lacking PbSERAser showed increased expression of the cysteine-type PbSERA3. Compensatory mechanisms between distinct SERA subfamilies may thus explain the absence of phenotypical defect in SERAser disruptants, and challenge the suitability to develop potent antimalarial drugs based on specific inhibitors of Plasmodium serine-type SERAs.

Published
2010

20. Global and 3D Spatial Assessment of Neuroinflammation in Rodent Models of Multiple Sclerosis

Author

Gupta, Shashank, Utoft, Regine Egeholm, Hasseldam, Henrik, Schmidt-Christensen, Anja, Hannibal, Tine Dahlbæk, Hansen, Lisbeth, Fransén Pettersson, Nina Isabell, Gupta, Noopur Agarwal, Rozell, Björn, Andersson, Åsa, Holmberg, Dan Ingemar, Gupta, Shashank, Utoft, Regine Egeholm, Hasseldam, Henrik, Schmidt-Christensen, Anja, Hannibal, Tine Dahlbæk, Hansen, Lisbeth, Fransén Pettersson, Nina Isabell, Gupta, Noopur Agarwal, Rozell, Björn, Andersson, Åsa, and Holmberg, Dan Ingemar

Abstract

Multiple Sclerosis (MS) is a progressive autoimmune inflammatory and demyelinating disease of the central nervous system (CNS). T cells play a key role in the progression of neuroinflammation in MS and also in the experimental autoimmune encephalomyelitis (EAE) animal models for the disease. A technology for quantitative and 3 dimensional (3D) spatial assessment of inflammation in this and other CNS inflammatory conditions is much needed. Here we present a procedure for 3D spatial assessment and global quantification of the development of neuroinflammation based on Optical Projection Tomography (OPT). Applying this approach to the analysis of rodent models of MS, we provide global quantitative data of the major inflammatory component as a function of the clinical course. Our data demonstrates a strong correlation between the development and progression of neuroinflammation and clinical disease in several mouse and a rat model of MS refining the information regarding the spatial dynamics of the inflammatory component in EAE. This method provides a powerful tool to investigate the effect of environmental and genetic forces and for assessing the therapeutic effects of drug therapy in animal models of MS and other neuroinflammatory/neurodegenerative disorders.

Published
2013

25. The Plasmodium serine-type SERA proteases display distinct expression patterns and non-essential in vivo roles during life cycle progression of the malaria parasite.

Author

Putrianti, Elyzana D., Schmidt-Christensen, Anja, Arnold, Iris, Heussler, Volker T., Matuschewski, Kai, and Silvie, Olivier

Subjects
*PROTEOLYTIC enzymes, *PLASMODIUM, *PARASITE life cycles, *HEMOGLOBINS, *GENE expression, *CYSTEINE proteinases, *ANTIMALARIALS
Abstract

Parasite proteases play key roles in several fundamental steps of the Plasmodium life cycle, including haemoglobin degradation, host cell invasion and parasite egress. Plasmodium exit from infected host cells appears to be mediated by a class of papain-like cysteine proteases called ‘serine repeat antigens’ (SERAs). A SERA subfamily, represented by Plasmodium falciparum SERA5, contains an atypical active site serine residue instead of a catalytic cysteine. Members of this SERAser subfamily are abundantly expressed in asexual blood stages, rendering them attractive drug and vaccine targets. In this study, we show by antibody localization and in vivo fluorescent tagging with the red fluorescent protein mCherry that the two P. berghei serine-type family members, PbSERA1 and PbSERA2, display differential expression towards the final stages of merozoite formation. Via targeted gene replacement, we generated single and double gene knockouts of the P. berghei SERAser genes. These loss-of-function lines progressed normally through the parasite life cycle, suggesting a specialized, non-vital role for serine-type SERAs in vivo. Parasites lacking PbSERAser showed increased expression of the cysteine-type PbSERA3. Compensatory mechanisms between distinct SERA subfamilies may thus explain the absence of phenotypical defect in SERAser disruptants, and challenge the suitability to develop potent antimalarial drugs based on specific inhibitors of Plasmodium serine-type SERAs. [ABSTRACT FROM AUTHOR]

Published
2010
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26. Expression and processing of Plasmodium berghei SERA3 during liver stages.

Author

Schmidt-Christensen, Anja, Sturm, Angelika, Horstmann, Sebastian, and Heussler, Volker T.

Subjects
*CYSTEINE proteinases, *PLASMODIUM, *LIVER cells, *CELL death, *CYTOPLASM, *IMMUNOFLUORESCENCE
Abstract

Cysteine proteases mediate liberation of Plasmodium berghei merozoites from infected hepatocytes. In an attempt to identify the responsible parasite proteases, we screened the genome of P. berghei for cysteine protease-encoding genes. RT-PCR analyses revealed that transcription of four out of five P. berghei serine repeat antigen (PbSERA) genes was strongly upregulated in late liver stages briefly before the parasitophorous vacuole membrane ruptured to release merozoites into the host cell cytoplasm, suggesting a role of PbSERA proteases in these processes. In order to characterize PbSERA3 processing, we raised an antiserum against a non-conserved region of the protein and generated a transgenic P. berghei strain expressing a TAP-tagged PbSERA3 under the control of the endogenous promoter. Immunofluorescence assays revealed that PbSERA3 leaks into the host cell cytoplasm during merozoite development, where it might contribute to host cell death or activate host cell proteases that execute cell death. Importantly, processed PbSERA3 has been detected by Western blot analysis in cell extracts of schizont-infected cells and merozoite-infected detached hepatic cells. [ABSTRACT FROM AUTHOR]

Published
2008
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