Format

Send to

Choose Destination
Parasitology. 2014 Apr;141(5):602-13. doi: 10.1017/S0031182013001984. Epub 2013 Dec 13.

The role of chemokines in severe malaria: more than meets the eye.

Author information

1
The Walter and Eliza Hall Institute of Medical Research, 1G Royal Parade, Parkville, Victoria 3052, Australia.
2
Burnet Institute, 85 Commercial Road, Melbourne, Victoria 3004, Australia.

Abstract

Plasmodium falciparum malaria is responsible for over 250 million clinical cases every year worldwide. Severe malaria cases might present with a range of disease syndromes including acute respiratory distress, metabolic acidosis, hypoglycaemia, renal failure, anaemia, pulmonary oedema, cerebral malaria (CM) and placental malaria (PM) in pregnant women. Two main determinants of severe malaria have been identified: sequestration of parasitized red blood cells and strong pro-inflammatory responses. Increasing evidence from human studies and malaria infection animal models revealed the presence of host leucocytes at the site of parasite sequestration in brain blood vessels as well as placental tissue in complicated malaria cases. These observations suggested that apart from secreting cytokines, leucocytes might also contribute to disease by migrating to the site of parasite sequestration thereby exacerbating organ-specific inflammation. This evidence attracted substantial interest in identifying trafficking pathways by which inflammatory leucocytes are recruited to target organs during severe malaria syndromes. Chemo-attractant cytokines or chemokines are the key regulators of leucocyte trafficking and their potential contribution to disease has recently received considerable attention. This review summarizes the main findings to date, investigating the role of chemokines in severe malaria and the implication of these responses for the induction of pathogenesis and immunity to infection.

PMID:
24476686
PMCID:
PMC3962270
DOI:
10.1017/S0031182013001984
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Cambridge University Press Icon for PubMed Central
Loading ...
Support Center