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Summary  Infection with the malaria parasite,  Plasmodium , is associated with a strong inflammatory response and parasite cytoadhesion (sequestration) in several organs. Here, we have carried out a systematic study of sequestration and histopathology during infection of C57Bl/6 mice with   P lasmodium chabaudi   AS  and determined the influence of the immune response. This parasite sequesters predominantly in liver and lung, but not in the brain, kidney or gut. Histopathological changes occur in multiple organs during the acute infection, but are not restricted to the organs where sequestration takes place. Adaptive immunity, and signalling through the IFNγ receptor increased sequestration and histopathology in the liver, but not in the lung, suggesting that there are differences in the adhesion molecules and/or parasite ligands utilized and mechanisms of pathogenesis in these two organs. Exacerbation of pro‐inflammatory responses during infection by deletion of the  il10  gene resultsin the aggravation of damage to lung and kidney irrespective of the degree of sequestration. The immune response therefore affected both sequestration and histopathology in an organ‐specific manner.  P. chabaudi   AS  provides a good model to investigate the influence of the host response on the sequestration and specific organ pathology, which is applicable to human malaria.

Sequestration and histopathology in P lasmodium chabaudi malaria are influenced by the immune response in an organ‐specific manner