Abstract

BackgroundPro- and anti-inflammatory cytokines are important mediators of immunity and are associated with malaria disease outcomes. However, their role in the establishment of asymptomatic infections, which may precede the development of clinical symptoms, is not as well-understood.MethodsWe determined the association of pro and anti-inflammatory cytokines and other immune effector molecules with the development of asymptomatic malaria. We measured and compared the plasma levels of pro-inflammatory mediators including tumor necrosis factor-alpha (TNF-α), interferon-gamma (IFN-γ), interleukin (IL)-6, IL-12p70, IL-17A, and granzyme B, the anti-inflammatory cytokine IL-4 and the regulatory cytokine IL-10 from children with asymptomatic malaria infections (either microscopic or submicroscopic) and uninfected controls using Luminex.ResultsWe show that individuals with microscopic asymptomatic malaria had significantly increased levels of TNF-α and IL-6 compared to uninfected controls. Children with either microscopic or submicroscopic asymptomatic malaria exhibited higher levels of IFN-γ, IL-17A, and IL-4 compared to uninfected controls. The levels of most of the pro and anti-inflammatory cytokines were comparable between children with microscopic and submicroscopic infections. The ratio of IFN-γ/IL-10, TNF-α/IL-10, IL-6/IL-10 as well as IFN-γ/IL-4 and IL-6/IL-4 did not differ significantly between the groups. Additionally, using a principal component analysis, the cytokines measured could not distinguish amongst the three study populations. This may imply that neither microscopic nor submicroscopic asymptomatic infections were polarized toward a pro-inflammatory or anti-inflammatory response.ConclusionThe data show that asymptomatic malaria infections result in increased plasma levels of both pro and anti-inflammatory cytokines relative to uninfected persons. The balance between pro- and anti-inflammatory cytokines are, however, largely maintained and this may in part, explain the lack of clinical symptoms. This is consistent with the generally accepted observation that clinical symptoms develop as a result of immunopathology involving dysregulation of inflammatory mediator balance in favor of pro-inflammatory mediators.

Highlights

  • Malaria is a protozoan infectious disease that puts more than 3 billion of the world’s population at risk (WHO, 2018)

  • The age distribution differed significantly between the study cohorts (p = 0.021); children with submicroscopic asymptomatic malaria were significantly older than uninfected children (p = 0.017) but not children with microscopic asymptomatic malaria

  • We observed increased levels of cytokines such as TNF-α and IL-6 in children with microscopic asymptomatic malaria, whereas, IFN-γ, IL17A, and IL-4 levels were increased in infected children with microscopic or submicroscopic asymptomatic malaria compared with uninfected controls

Read more

Summary

Introduction

Malaria is a protozoan infectious disease that puts more than 3 billion of the world’s population at risk (WHO, 2018). A significant number of parasite-infected persons in malaria-endemic areas are asymptomatic (Bousema et al, 2014; Snow et al, 2017) These asymptomatic infections are loosely defined as individuals who present with parasites over a period of time but have no clinical symptoms of the disease and have not recently been treated with anti-malarial drugs (Lindblade et al, 2013). Pro- and anti-inflammatory cytokines are important mediators of immunity and are associated with malaria disease outcomes Their role in the establishment of asymptomatic infections, which may precede the development of clinical symptoms, is not as well-understood

Methods
Results
Discussion
Conclusion

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.