AI Article Synopsis

  • * The study shows that malaria infection weakens the body's inflammatory response to NTS, increasing bacterial colonization due to the malaria-induced production of IL-10.
  • * Mice lacking certain immune cell functions related to IL-10 were better at fighting off Salmonella infections, indicating that IL-10 from malaria hampers the immune system's ability to combat the bacteria.

Article 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.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4006898PMC
http://dx.doi.org/10.1371/journal.ppat.1004049DOI Listing

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