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BCG-malaria co-Infection has paradoxical effects on C57BL/6 and A/J mouse strains
Bacillus Calmette-Guérin (BCG) infection of the spleen is a potent modifier of splenic function. Prior to malaria infection, we infected two mouse strains of differing susceptibility to Plasmodium chabaudi AS (C57BL/6 and A/J) with this mycobacterium. We then evaluated aspects of spleen cell composi...
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Published in: | Parasite immunology 2008, Vol.30 (1), p.1-12 |
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Main Authors: | , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Bacillus Calmette-Guérin (BCG) infection of the spleen is a potent modifier of splenic function. Prior to malaria infection, we infected two mouse strains of differing susceptibility to Plasmodium chabaudi AS (C57BL/6 and A/J) with this mycobacterium. We then evaluated aspects of spleen cell composition, architecture and cytokine expression, and correlated these with the outcome. BCG preinfection resulted in protection of the A/J mice but paradoxically resulted in mortality of the C57BL/6 mice. The latter developed higher parasitaemias that peaked earlier than the A/J mice rendered resistant by BCG. BCG infection induced remarkable changes to splenic histology examined by H&E staining, but there were no consistent differences between mouse strains. C57BL/6 mice had higher absolute numbers of all immune cell phenotypes than did A/J mice, and higher macrophage and dendritic cell proportions. BCG-induced resistance in A/J mice was associated with an increased CD4⁺ expression of IFN-γ whilst induced death in C57BL/6 mice was associated with excessive IFN-γ expression. A moderate TH1 response in the A/J model may have been responsible for the improved survival, and an excessive TH1 response in the C57BL/6 model may have contributed to their death. |
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ISSN: | 0141-9838 1365-3024 |
DOI: | 10.1111/j.1365-3024.2007.00983.x |