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Background  Parasite cytoadherence within the microvasculature of tissues and organs of infected individuals is implicated in the pathogenesis of several malaria syndromes. Multiple host receptors may mediate sequestration. The identity of the host receptor(s), or the parasite ligand(s) responsible for sequestration of  Plasmodium  species other than  Plasmodium falciparum  is largely unknown. The rodent malaria parasites may be useful to model interactions of parasite species, which lack the  var  genes with their respective hosts, as other multigene families are shared between the species. The role of the endothelial receptors ICAM-1 and CD36 in cytoadherence and in the development of pathology was investigated in a  Plasmodium chabaudi  infection in C57BL/6 mice lacking these receptors. The schizont membrane-associated cytoadherence (SMAC) protein of  Plasmodium berghei  has been shown to exhibit reduced CD36-associated cytoadherence in  P. berghei  ANKA-infected mice.    Methods  Parasite tissue sequestration and the development of acute stage pathology in  P. chabaudi  infections of mice lacking CD36 or ICAM-1, their respective wild type controls, and in infections with mutant  P. chabaudi  parasites lacking the  smac  gene were compared. Peripheral blood parasitaemia, red blood cell numbers and weight change were monitored throughout the courses of infection. Imaging of bioluminescent parasites in isolated tissues (spleen, lungs, liver, kidney and gut) was used to measure tissue parasite load.    Results  This study shows that neither the lack of CD36 nor the deletion of the  smac  gene from  P. chabaudi  significantly impacted on acute-stage pathology or parasite sequestration. By contrast, in the absence of ICAM-1, infected animals experience less anaemia and weight loss, reduced parasite accumulation in both spleen and liver and higher peripheral blood parasitaemia during acute stage malaria. The reduction in parasite tissue sequestration in infections of ICAM-1 null mice is maintained after mosquito transmission.    Conclusions  These results indicate that ICAM-1-mediated cytoadherence is important in the  P. chabaudi  model of malaria and suggest that for rodent malarias, as for  P. falciparum , there may be multiple host and parasite molecules involved in sequestration.    Electronic supplementary material  The online version of this article (doi:10.1186/s12936-017-1834-8) contains supplementary material, which is available to authorized users.

ICAM-1 is a key receptor mediating cytoadherence and pathology in the Plasmodium chabaudi malaria model