Psychoneuroendocrine stress response may impair neutrophil function in complex regional pain syndrome

Abstract In order to elucidate the interaction between pain, stress and innate immunity in complex regional pain syndrome (CRPS), we assessed pain and stress levels in CRPS patients and compared ex vivo functions of neutrophils between patients with CRPS and healthy volunteers. As compared with healthy volunteers, the following major alterations in CRPS patients were found: (I) elevated stress score (PTSS-10) and stress hormone concentrations, (II) decreased expression of the CD62L and CD11b/CD18 on neutrophils, (III) impaired ability of autologous plasma to enhance the capability of neutrophils to phagocytose zymosan particles, and (IV) a negative correlation between PTSS-10 values and autologous plasma enhanced phagocytosis. In vitro incubation of neutrophils with catecholamines decreased phagocytosis of zymosan. In conclusion, CRPS patients exhibit signs of impaired innate immunity which might reflect the immunological consequence of an immunosuppressive neuroendocrine stress response.