Journal
MICROBES AND INFECTION
Volume 12, Issue 11, Pages 864-874Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.micinf.2010.05.013
Keywords
Malaria; Tuberculosis; Mycobacteria; Co-infection
Categories
Funding
- CIHR [MT-13721, MOP-15107, MOP-82772]
- Genome Canada through the Ontario Genomics Institute
- CIHR Canada Research Chairs
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Tuberculosis (Mtb) and malaria are among the most important infectious causes of morbidity and mortality worldwide, causing an estimated 1.5 million and 1 million deaths every year, respectively. Here we demonstrate a biological interaction between malaria and mycobacteria in vitro and in vivo. Murine macrophages co-incubated with Plasmodium falciparum parasitized erythrocytes demonstrated impaired control of intracellular Mtb replication, and reduced production of reactive nitrogen species in response to mycobacteria. Infection of C57BL/6 mice with Plasmodium species exacerbated the course of acute mycobacterial infection (57% increase in peak splenic CFU, p = 0.043 for difference over time course of infection), induced disruption of the structural integrity of established granulomas, and caused reactivation of latent mycobacterial infection (2.6-fold increase in peak splenic CFU, p = 0.016 for difference over time course of reactivation). Malaria pigment deposition within the granulomas of co-infected mice suggested that the influx of dysfunctional hemozoin-laden monocytes into the locus of mycobacterial control may contribute to impaired containment of mycobacteria. Collectively, these results point to malaria-induced dysregulation of innate and adaptive anti-mycobacterial defences, and suggest that the interaction of these globally important pathogens may potentiate Mtb infection and transmission. (C) 2010 Institut Pasteur. Published by Elsevier Masson SAS. All rights reserved.
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