Role of CD40-CVD40L in mouse severe malaria
| Autor: | Pierre F. Piguet, Anne Rochat, Chen Da Kan, Yves Donati, Constance Barazzone, Christian Vesin |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2001 |
| Předmět: |
RNA
Messenger/genetics CD40 Ligand/genetics/physiology Transcription Genetic Plasmodium berghei Parasitemia ddc:616.07 Mice 0302 clinical medicine ddc:590 Malaria/blood/immunology/pathology Platelet CD154 Mice Knockout Tumor Necrosis Factor-alpha/metabolism 0303 health sciences ddc:618 biology Antigens CD40/genetics/physiology Brain hemic and immune systems Intercellular Adhesion Molecule-1 3. Good health medicine.anatomical_structure Blood-Brain Barrier Tumor necrosis factor alpha Macrophages/physiology CD40 Ligand chemical and pharmacologic phenomena Blood–brain barrier Pathology and Forensic Medicine Andrology 03 medical and health sciences parasitic diseases medicine Animals RNA Messenger CD40 Antigens ddc:612 Intercellular Adhesion Molecule-1/genetics 030304 developmental biology CD40 Lung Gene Expression Regulation/immunology Tumor Necrosis Factor-alpha Platelet Count Macrophages biology.organism_classification medicine.disease Thrombocytopenia Malaria Mice Inbred C57BL Gene Expression Regulation Immunology biology.protein Brain/immunology/pathology Regular Articles 030215 immunology |
| Zdroj: | American Journal of Pathology, Vol. 159, No 2 (2001) pp. 733-42 |
| ISSN: | 0002-9440 |
| Popis: | We explored the role of CD40-CD40L (CD154) in the severe malaria elicited by Plasmodium berghei anka infection in mice. Mortality was >90% by day 8 after infection in +/+ mice, but markedly decreased in CD40−/− or in CD40L−/− mice, as well as in +/+ mice treated with anti-CD40L monoclonal antibody. Parasitemia was similar in the different conditions. Breakdown of the blood-brain barrier was evident in infected +/+, but not in CD40−/− mice. Thrombocytopenia was less severe in CD40−/− mice than in the +/+ controls. Sequestration of macrophages in brain venules and alveolar capillaries was reduced in CD40−/− or in CD40L−/− mice, whereas sequestration of parasitized red blood cells or polymorphonuclear leukocytes in alveolar capillaries was CD40-CD40L-independent. CD40 mRNA was increased in the brain and lung of infected mice whereas CD40L was increased in the lung. Tumor necrosis factor plasma levels were similarly increased in infected +/+ or CD40−/− mice. Expression of CD54 and its mRNA levels in the brain were moderately decreased in CD40-deficient mice. Thus the mortality associated with severe malaria requires CD40-CD40L interaction that contributes to the breakdown of the blood-brain barrier, macrophage sequestration, and platelet consumption. |
| Databáze: | OpenAIRE |
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