Coccidian Infection Causes Oxidative Damage in Greenfinches

The main tenet of immunoecology is that individual variation in immune responsiveness is caused by the costs of immune responses to the hosts. Oxidative damage resulting from the excessive production of reactive oxygen species during immune response is hypothesized to form one of such costs. We tested this hypothesis in experimental coccidian infection model in greenfinches Carduelis chloris. Administration of isosporan coccidians to experimental birds did not affect indices of antioxidant protection (TAC and OXY), plasma triglyceride and carotenoid levels or body mass, indicating that pathological consequences of infection were generally mild. Infected birds had on average 8% higher levels of plasma malondialdehyde (MDA, a toxic end-product of lipid peroxidation) than un-infected birds. The birds that had highest MDA levels subsequent to experimental infection experienced the highest decrease in infection intensity. This observation is consistent with the idea that oxidative stress is a causative agent in the control of coccidiosis and supports the concept of oxidative costs of immune responses and parasite resistance. The finding that oxidative damage accompanies even the mild infection with a common parasite highlights the relevance of oxidative stress biology for the immunoecological research

Antioxidant protection, carotenoids and coccidians in greenfinches – assessment of the costs of immune activation and mechanisms of parasite resistance in a passerine with carotenoid-based ornaments

Autoriõigustest tulenevatel põhjustel on ligipääs piiratu

Effects of Endotoxin and Psychological Stress on Redox Physiology, Immunity and Feather Corticosterone in Greenfinches

Assessment of costs accompanying activation of immune system and related neuroendocrine pathways is essential for understanding the selective forces operating on these systems. Here we attempted to detect such costs in terms of disruption to redox balance and interference between different immune system components in captive wild-caught greenfinches (Carduelis chloris). Study birds were subjected to an endotoxin-induced inflammatory challenge and temporary exposure to a psychological stressor (an image of a predator) in a 2*2 factorial experiment. Injection of bacterial endotoxin resulted in up-regulation of two markers of antioxidant protection - erythrocyte glutathione, and plasma oxygen radical absorbance (OXY). These findings suggest that inflammatory responses alter redox homeostasis. However, no effect on markers of oxidative damage to proteins or DNA in erythrocytes could be detected. We found no evidence that the endotoxin injection interfered with antibody production against Brucella abortus antigen or the intensity of chronic coccidiosis. The hypothesis of within-immune system trade-offs as a cost of immunity was thus not supported in our model system. We showed for the first time that administration of endotoxin can reduce the level of corticosterone deposited into feathers. This finding suggests a down-regulation of the corticosterone secretion cascade due to an endotoxin-induced immune response, a phenomenon that has not been reported previously. Exposure to the predator image did not affect any of the measured physiological parameters

Effects of experimental coccidian infection on changes of body mass and biochemical parameters of greenfinches between first and second blood sampling.

<p>η² stands for coefficients of partial determination, describing the proportion of total variation attributable to the predictor variable, partialling out other factors from the total nonerror variation. Average trait values are presented in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0036495#pone-0036495-t001" target="_blank">Table 1</a>.</p

Biochemical indices and body mass of greenfinches at first and second blood sampling (before and after experimental infection).

<p>Biochemical indices and body mass of greenfinches at first and second blood sampling (before and after experimental infection).</p

Relationship between change in infection intensity between day 44 (last sampling of infection) and day 24 (before infecting) and plasma MDA levels at second blood sampling in an ANCOVA adjusting for a initial value of infection intensity and infection treatment. Interaction terms with infection treatment were not significant (P>0.9).

<p>Relationship between change in infection intensity between day 44 (last sampling of infection) and day 24 (before infecting) and plasma MDA levels at second blood sampling in an ANCOVA adjusting for a initial value of infection intensity and infection treatment. Interaction terms with infection treatment were not significant (P>0.9).</p

Timeline of the experiment and dynamic of the infection.

<p>Day 1 = 4 January. Effect of treatment: F_1,54 = 13.2, P = 0.006; Effect of time: F_6,324 = 52.9, P<0.00001; Effect of time*treatment F_6,324 = 36.3, P<0.00001. Average infection intensities did not differ between infected and not infected birds before infecting (P = 0.6–1), while after infecting, infected group had significantly higher oocyst shedding in any date of measurement (P = 0.03–0.0001).</p