Abstract
Background Plasmodium parasites may affect the oxidative status of their hosts, defined as the balance of pro-oxidant compounds and antioxidant defences in an organism. An increased energy requirement, the activation of immune functions or the parasite itself may lead to a higher production of pro-oxidants and/or an antioxidant depletion resulting in a higher oxidative stress and associated damage in infected individuals. Relatively little is known about the mechanisms underlying oxidative processes at play during host-Plasmodium interaction in the wild.MethodsThe effect of Plasmodium infection on host oxidative status was investigated in wild populations of breeding great tits, Parus major, naturally infected by Plasmodium spp. When chicks were 14 days old, the parents were blood-sampled to measure four complementary oxidative status markers: pro-oxidant production as mitochondrial superoxide production in red blood cells (RBC), antioxidant defences as plasma antioxidant capacity and oxidative damage as reactive oxygen metabolites in the plasma and RBC membrane resistance to oxidative attack.Results Plasmodium-infected individuals produced more pro-oxidants compared to uninfected ones and pro-oxidant production positively correlated to infection intensity. There was also a conditional effect of reproductive effort on oxidative damage depending on Plasmodium infection status. There was no direct effect of infection on oxidative damage and no effect on antioxidant defences.ConclusionsThe results suggest that Plasmodium parasites may impose a cost in terms of increased oxidative stress possibly mediated via a higher energy requirement in infected hosts. This further suggests that Plasmodium parasites may modify host life history traits via an induction of oxidative stress. This study highlights that measuring several complementary oxidative status markers may enable to capture oxidative processes at play during host-Plasmodium interactions.Electronic supplementary materialThe online version of this article (doi:10.1186/s12936-016-1579-9) contains supplementary material, which is available to authorized users.
Highlights
Plasmodium parasites may affect the oxidative status of their hosts, defined as the balance of prooxidant compounds and antioxidant defences in an organism
Plasmodium parasites, which cause malaria, are ubiquitous parasites infecting a wide range of vertebrate species [1] on which they impose fitness costs ranging from decreased survival [2,3,4], decreased fecundity [5] to lower levels of disease severity [6, 7]
This is the first time an red blood cells (RBC) superoxide production increase is reported in wild Plasmodium-infected animals and this result is in line with results from in vitro studies that have shown that there is an increase in pro-oxidant levels in Plasmodium-infected RBCs [31]
Summary
Plasmodium parasites may affect the oxidative status of their hosts, defined as the balance of prooxidant compounds and antioxidant defences in an organism. The activation of immune functions or the parasite itself may lead to a higher production of pro-oxidants and/or an antioxidant depletion resulting in a higher oxidative stress and associated damage in infected individuals. Regardless of the direct fitness cost of parasite infection, malaria induces physiological changes in hosts, which may subsequently affect a host’s oxidative status. Parasites may divert host resources for their own development, increasing host energy requirement and prooxidant production and/or depleting host antioxidant resources. Parasites may induce sickness behaviour during which the hosts will reallocate energy/ resources away from secondary activities, such as locomotion or reproduction, towards immune functions [19]. Infected individuals have been shown to increase their reproductive investment when they were experimentally cleared of an infection [5]
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