Abstract HNPs produced by neutrophils at the bacterial translocation site play an important role on controlling gut bacteria-associated infections. However, these peptides were not produced by burn patient neutrophils. CCL2 released from burn patient neutrophils was shown to be inhibitory on HNP production. In this study, we tried to recover the impaired production of HNPs in cultures of neutrophils isolated from severely burned patients. Neutrophils (1 x 106 cells/ml), isolated from peripheral blood of severely burned patients and healthy donors, were cultured in media supplemented with burn patient sera (10% v/v) and/or various doses of GL (Minophagen Pharmaceutical Co., Ltd., Tokyo, Japan). Culture fluids were harvested 18 hrs after cultivation and assayed for HNPs by ELISA. In the results, a 28 to 37 ng/ml of HNPs was detected in culture media of healthy donor neutrophils, while these peptides were not produced by burn patient neutrophils. However, HNPs were detected in cultures of burn patient neutrophils treated with 10 to 100 μg/ml of GL. HNPs were not produced by healthy donor neutrophils in cultures supplemented with burn patient sera, and CCL2 was detected in these sera. This chemokine was shown to be inhibitory on HNP production by healthy donor neutrophils. CCL2 was not produced by burn patient neutrophils treated with GL. These results indicate that GL improves HNP production by burn patient neutrophils through the control of CCL2 production.