Although stress is linked to asthma exacerbation, underlying mechanisms are unclear. Given the shared relevance to stress and asthma, select neuroendocrine and immune responses to acute stressors and their impact on pulmonary function were examined, comparing responses between students with (n = 20) and without childhood asthma (n = 16). Students were challenged with speech and math tasks. Blood samples were collected five times: before tasks, immediately after first and second tasks, and 15 and 60 minutes posttasks. Pulmonary function was measured four times, excluding midtask point. Stress reactivity patterns did not differ between two groups. However, all measures showed significant changes across the challenge. Plasma epinephrine and norepinephrine rose during tasks and declined after tasks, p < .001. Cortisol mainly declined after tasks, p = .03. Leukocyte count increased during tasks with increased lymphocyte percentage that declined after tasks, while neutrophil percentage changed opposite to lymphocytes, p < .001 each. Changes in pulmonary function were significant, p < .05, but were not predicted by the magnitude of neuroendocrine and immune changes. Instead, neuroendocrine and immune levels explained 33%-51% of variance on concurrent pulmonary function. Findings indicate that acute stress induces significant neuroendocrine and immune changes that can affect pulmonary function. However, stress reactivity needs further investigation with larger samples and people with a more severe form of asthma.