Premium
BCG–malaria co‐Infection has paradoxical effects on C57BL/6 and A/J mouse strains
Author(s) -
LEISEWITZ A.L.,
ROCKETT K.,
KWIATKOWSKI D.
Publication year - 2008
Publication title -
parasite immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.795
H-Index - 75
eISSN - 1365-3024
pISSN - 0141-9838
DOI - 10.1111/j.1365-3024.2007.00983.x
Subject(s) - plasmodium chabaudi , biology , spleen , immunology , immune system , c57bl/6 , malaria , immunity , virology , plasmodium falciparum , parasitemia
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.