Journal article
Kristen L Lokken, Jason P Mooney, B. P. Butler, M. N. Xavier, J. Chau, Nicola Schaltenberg, R. H. Begum, Werner Müller, S. Luckhart, R. Tsolis
PLoS pathogens, 2014
PLoS pathogens, 2014
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APA
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Lokken, K. L., Mooney, J. P., Butler, B. P., Xavier, M. N., Chau, J., Schaltenberg, N., … Tsolis, R. (2014). Malaria Parasite Infection Compromises Control of Concurrent Systemic Non-typhoidal Salmonella Infection via IL-10-Mediated Alteration of Myeloid Cell Function. PLoS Pathogens.
Chicago/Turabian
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Lokken, Kristen L, Jason P Mooney, B. P. Butler, M. N. Xavier, J. Chau, Nicola Schaltenberg, R. H. Begum, Werner Müller, S. Luckhart, and R. Tsolis. “Malaria Parasite Infection Compromises Control of Concurrent Systemic Non-Typhoidal Salmonella Infection via IL-10-Mediated Alteration of Myeloid Cell Function.” PLoS pathogens (2014).
MLA
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Lokken, Kristen L., et al. “Malaria Parasite Infection Compromises Control of Concurrent Systemic Non-Typhoidal Salmonella Infection via IL-10-Mediated Alteration of Myeloid Cell Function.” PLoS Pathogens, 2014.
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@article{kristen2014a,
title = {Malaria Parasite Infection Compromises Control of Concurrent Systemic Non-typhoidal Salmonella Infection via IL-10-Mediated Alteration of Myeloid Cell Function},
year = {2014},
journal = {PLoS pathogens},
author = {Lokken, Kristen L and Mooney, Jason P and Butler, B. P. and Xavier, M. N. and Chau, J. and Schaltenberg, Nicola and Begum, R. H. and Müller, Werner and Luckhart, S. and Tsolis, R.}
}
Abstract
Non-typhoidal Salmonella serotypes (NTS) cause a self-limited gastroenteritis in immunocompetent individuals, while children with severe Plasmodium falciparum malaria can develop a life-threatening disseminated infection. This co-infection is a major source of child mortality in sub-Saharan Africa. However, the mechanisms by which malaria contributes to increased risk of NTS bacteremia are incompletely understood. Here, we report that in a mouse co-infection model, malaria parasite infection blunts inflammatory responses to NTS, leading to decreased inflammatory pathology and increased systemic bacterial colonization. Blunting of NTS-induced inflammatory responses required induction of IL-10 by the parasites. In the absence of malaria parasite infection, administration of recombinant IL-10 together with induction of anemia had an additive effect on systemic bacterial colonization. Mice that were conditionally deficient for either myeloid cell IL-10 production or myeloid cell expression of IL-10 receptor were better able to control systemic Salmonella infection, suggesting that phagocytic cells are both producers and targets of malaria parasite-induced IL-10. Thus, IL-10 produced during the immune response to malaria increases susceptibility to disseminated NTS infection by suppressing the ability of myeloid cells, most likely macrophages, to control bacterial infection.
