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| Author(s): |
Lara do Amaral Silva
Total Authors: 1
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| Document type: | Doctoral Thesis |
| Press: | Jaboticabal. 2020-09-26. |
| Institution: | Universidade Estadual Paulista (Unesp). Faculdade de Ciências Agrárias e Veterinárias. Jaboticabal |
| Defense date: | 2020-09-21 |
| Advisor: | Kênia Cardoso Bícego |
| Abstract | |
Although thermal responses to pathogen infections are decisive for birds’ survival, the mechanisms of fever are largely unknown and no study has addressed the decrease in body temperature during systemic inflammation for birds. Here we challenged Gallus gallus chicks with high doses of endotoxin to study the physiological and biochemical mechanisms of birds’ thermoregulation during systemic inflammation. Firstly, we described the decrease in body temperature during systemic inflammation in birds as a regulated response (anapyrexia). This response was supported by a thermogenesis inhibition (reduced metabolic rate) unrelated to impairment of mitochondrial function or oxygen supply, and also by heat loss mechanisms, such as tachypnea and vasodilation. In sequence, we presented that anapirexia in response to endotoxin was independent of cyclooxygenases mediation (COX), thus the prostaglandin (PG) profile observed during this response did not reflect a thermal function. Moreover, the fever response depended specifically on COX-2 signaling in our chicks, and when it was blocked fever was eliminated by inhibition of heat loss mechanisms such as vasoconstriction and huddling behavior. Yet, fever seems to be mostly dependent on PGE2 signaling, but PGD2 and PGF2 had also a minor increase in expression during fever. Our data also pointed out that competing energetic demands caused by cold, and cold combined with fasting favors anapyrexia and eliminates the fever response in chicks. Finally, we show that the exposure of chicks to the pollutant dioxin during embryonic development resulted in increased in metabolic rate. Thus, when inflammation was induced, these chicks showed a persistent hypometabolic response accompanied by the elimination of normal hematological and osmotic responses to endotoxin. We conclude that chicks can respond to an immune challenge with both anapyrexia and fever, and the anapyretic response is favored in case of increased metabolic demands. Furthermore, anapyrexia is not mediated by the COX-PG pathway, whereas fever is mediated specifically by COX-2 and mainly by PGE2. (AU) | |
| FAPESP's process: | 17/00864-6 - Physiological and biochemical mechanisms of thermal response to systemic inflammation in chicks |
| Grantee: | Lara do Amaral Silva |
| Support Opportunities: | Scholarships in Brazil - Doctorate |