Developmental conditions may impact the expression of immune traits throughout an individual's life. Early-life challenges may lead to immunological constraints that are mediated by endocrine-immune interactions. In particular, individual differences in the ability to mount immune responses may be programmed by exposure to stressors or glucocorticoid hormones during development. To test this hypothesis, we experimentally elevated levels of the glucocorticoid hormone corticosterone during the nestling and fledgling periods in captive zebra finches (Taeniopygia guttata). We subsequently challenged birds with the antigen lipopolysaccharide (LPS) on days 60 and 100 posthatch to determine if developmental exposure to elevated corticosterone impacted the later response to LPS. As measures of immune function, we quantified bacteria killing ability (BKA), haptoglobin concentrations, and LPS-specific antibody responses at multiple time points. We also measured circulating corticosterone concentrations during the experimental period and on day 60 before and after endotoxin challenge. During the experimental period, corticosterone treatment elevated corticosterone levels. Corticosterone treatment did not induce programming effects on immune function or corticosterone production. Independent of treatment, individuals with higher corticosterone concentrations during the nestling period had lower BKA on day 36 and higher baseline corticosterone concentrations on day 60 posthatch. These results suggest a limited role for corticosterone exposure during early life to mediate immunological constraints later in life. Manipulation of cortisol may be necessary to conclusively determine if developmental glucocorticoid exposure can program immune function in birds. To determine if developmental stress can program the immune response, exposure to environmentally relevant stressors should also be manipulated.