Gail L. McCormick, Travis R. Robbins, Sonia A. Cavigelli, and Tracy Langkilde
Early life stress can suppress immune function, but it is unclear if transgenerational stress exposure modulates the immune consequences of early stress. In populations where, historically, the immune system is frequently activated, e.g. persistent stressors that cause injury, it may be maladaptive to suppress immune function after early life stress. Thus, the relationship between early life stress and immune function may vary with population-level historical stressor exposure. We collected gravid fence lizards (Sceloporus undulatus) from populations that naturally differ in long-term exposure to invasive fire ants (Solenopsis invicta). We manipulated early life stress in resulting offspring via weekly exposure to fire ants, application of the stress-relevant hormone corticosterone, or control treatment from 2 to 43 weeks of age. We quantified adult immune function in these offspring with baseline and antigen-induced hemagglutination and plasma bacterial killing ability. Early life corticosterone exposure suppressed baseline hemagglutination in offspring of lizards from populations without fire ants but enhanced hemagglutination in those from populations with fire ants. This enhancement may prepare lizards for high rates of wounding, toxin exposure, and infection associated with fire ant attack. Adult bacterial killing ability and hemagglutination were not affected by early life exposure to fire ants, but the latter was higher in offspring of lizards from invaded sites. A population’s history of persistent wounding may thus alter individual long-term immunological responses to early life stressors. Further consideration of historical stressor exposure (type and duration) may be important to better understand how early life stressors affect adult physiology.