COMBINED EFFECTS OF AMBIENT TEMPERATURE AND FOOD AVAILABILITY ON INDUCED INNATE IMMUNE RESPONSE OF A FRUIT-EATING BAT (CAROLLIA PERSPICILLATA)

Abstract

Resilience of mammals to anthropogenic climate and land-use changes is associated with the maintenance of adequate responses of several fitness-related traits such as those related to immune functions. The combined effects of decrease in food availability (Fa) and an increase in ambient temperature (Ta) can lead to immunosuppression and greater susceptibility to disease. In this study, we measured how selected physiological and behavioral components associated with the innate immune system of fruit-eating bats (Carollia perspicillata) respond to isolated and combined effects of changes in Ta and Fa. We tested the general hypothesis that decreased Fa, increased Ta and the combined effect of both factors would affect bat immune performance. Physiological (fever, leukocytosis and neutrophil/lymphocyte ratio) and behavioral (food intake) components of the acute phase response (APR), as well as bacterial killing ability of the plasma (BKA) were assessed after immune challenge with lipopolysaccharide (LPS: 10 mg/kg) in experimental groups kept at different short-term conditions of Fa (ad libitum diet or 50% food-deprived) and Ta (27 and 33°C). Our results indicate that magnitude of increase in body temperature was not affected by Fa, Ta or the interaction of both factors, but the time to reach the highest increase took longer in LPS-injected bats that were kept under food restriction. The magnitude of increased neutrophil/lymphocyte ratio (N/L) was affected by the interaction between Fa and Ta, but food intake, total white blood cell count and BKA were not affected by any factor or interaction. Overall, our results suggest that BKA and most components of APR examined are not affected by short-term changes in Fa and Ta within the range evaluated in this study, and that the increase of the N/L ratio when bats are exposed to low Fa and high Ta might represent an enhancement of cellular response to deal with infection.